Duration of Action of Inhaled vs. Intravenous β2-Adrenoceptor Agonists in an Anaesthetized Guinea-pig Model

We compared the duration of action of the short-acting α₂-adrenoceptor agonist salbutamol and the long-acting α₂-adrenoceptor agonists salmeterol and formoterol when administered iv or by inhalation in a histamine-induced bronchoconstriction model in the guinea-pig. Following aerosol dosing, maximal bronchoprotector effects were seen for salbutamol, salmeterol and formoterol at concentrations of 1 mg/ml, 100 μ g/ml and 30 μ g/ml respectively, giving a potency order of formoterol > salmeterol > salbutamol. All displayed similar maximum effects in this system. A maximal concentration of salbutamol showed bronchoprotection at 1 h but not at 3 h post-dosing whereas maximal concentrations of formoterol and salmeterol showed protection up to 5 h post-aqueous-aerosol dosing, giving a duration order of salmeterol > formoterol > salbutamol. All three α₂-adrenoceptor agonists showed dose-dependent bronchoprotection and duration of action following intravenous administration; salbutamol and salmeterol were equipotent and both were less potent than formoterol. Bronchoprotection obtained with sub-maximal concentrations of all three α₂-adrenoceptor agonists faded within 30 min following iv administration, but this could be extended by increasing the doses. These results demonstrate that the route of administration is important in determining the duration of action of α₂-adrenoceptor agonists in the lung. Furthermore, such findings lend support to the suggestion that the physico-chemical characteristics of salmeterol govern its duration of action rather than sustained binding of this agonist to a α₂-adrenoceptor exo-site.     

Peripheral T cell receptors αβ and γδ in patients with Hodgkin's lymphoma

Antigen recognition by T cells is determined by an antigen specific T cell receptor (TCR). Two heterodimeric TCR structures associated with CD3 have been defined: TCR αβ and TCR γδ. TCR αβ and its function are well described but the role of TCR γδ in normal and lymphoproliferative disorders is not well established. In newly diagnosed or relapsed/refractory Hodgkin's disease (HD), a disease associated with defective T cell functions and increased sIL-2R, We determined levels of seven TCR αβ variable regions [βV5(a), βV5(b), βV6(a), βV12(a), αβV(a), αV2(a)] and TCR γδ by using monoclonal antibodies (MCA). TCR γδ levels did not show any difference, but several variable regions of the TCR αβ differed when groups are compared with each other and the control group.     

Association of β2-adrenoceptor Gln27Glu variant with body weight but not hypertension

β₂-Adrenoceptor (β₂-ADR)-mediated vasodilatation decreases vascular reactivity and blood pressure (BP) and chromosome 5 where its gene (ADRB2R) resides and shows linkage to hypertension (HT). A Gln27Glu ADRB2R variant confers resistance to agonist-induced desensitization and enhanced vasodilator response to isoprenaline. Therefore, we carried out a case-control study in a cohort of HT and normotensive (NT) Anglo-Celtic Australian white subjects whose parents had a similar BP status as the subjects. Glu27 frequency was 0.41 in 108 HT and 0.42 in 141 NT (χ² = 0.05, P = .82). Within the HT group, the Glu27 allele was more prevalent in 61 subjects who were overweight (body mass index [BMI] ≥ 25 kg/m²) compared with 41 who were lean (BMI <25 kg/m²); ie, 0.49 v 0.31, respectively (χ² = 6.4, P = .012). Furthermore, Glu27 tracked with elevation in BMI in these subjects: 24 ± 4 kg/m², 27 ± 5 kg/m², and 28 ± 5 kg/m² for Gln/Gln, Gln/Glu, and Glu/Glu, respectively (P = .0058 by one-way ANOVA). Thus, the Gln27Glu β₂-ADR variant is excluded in HT, but might influence body weight.     

Dysfunction of ouabain-induced cardiac contractility in mice with heart-specific ablation of Na,K-ATPase β1-subunit

Na,K-ATPase is composed of two essential α- and β-subunits, both of which have multiple isoforms. Evidence indicates that the Na,K-ATPase enzymatic activity as well as its α₁, α₃ and β₁ isoforms are reduced in the failing human heart. The catalytic α-subunit is the receptor for cardiac glycosides such as digitalis, used for the treatment of congestive heart failure. The role of the Na,K-ATPase β₁-subunit (Na,K-β₁) in cardiac function is not known. We used Cre/loxP technology to inactivate the Na,K-β₁ gene exclusively in the ventricular cardiomyocytes. Animals with homozygous Na,K-β₁ gene excision were born at the expected Mendelian ratio, grew into adulthood, and appeared to be healthy until 10 months of age. At 13–14 months, these mice had 13% higher heart/body weight ratios, and reduced contractility as revealed by echocardiography compared to their wild-type (WT) littermates. Pressure overload by transverse aortic constriction (TAC) in younger mice, resulted in compensated hypertrophy in WT mice, but decompensation in the Na,K-β₁ KO mice. The young KO survivors of TAC exhibited decreased contractile function and mimicked the effects of the Na,K-β₁ KO in older mice. Further, we show that intact hearts of Na,K-β₁ KO anesthetized mice as well as isolated cardiomyocytes were insensitive to ouabain-induced positive inotropy. This insensitivity was associated with a reduction in NCX1, one of the proteins involved in regulating cardiac contractility. In conclusion, our results demonstrate that Na,K-β₁ plays an essential role in regulating cardiac contractility and that its loss is associated with significant pathophysiology of the heart.     

SARS-CoV-2 Infects Human ACE2-Negative Endothelial Cells through an αvβ3 Integrin-Mediated Endocytosis Even in the Presence of Vaccine-Elicited Neutralizing Antibodies

Integrins represent a gateway of entry for many viruses and the Arg-Gly-Asp (RGD) motif is the smallest sequence necessary for proteins to bind integrins. All Severe Acute Respiratory Syndrome Virus type 2 (SARS-CoV-2) lineages own an RGD motif (aa 403–405) in their receptor binding domain (RBD). We recently showed that SARS-CoV-2 gains access into primary human lung microvascular endothelial cells (HL-mECs) lacking Angiotensin-converting enzyme 2 (ACE2) expression through this conserved RGD motif. Following its entry, SARS-CoV-2 remodels cell phenotype and promotes angiogenesis in the absence of productive viral replication. Here, we highlight the α_vβ₃ integrin as the main molecule responsible for SARS-CoV-2 infection of HL-mECs via a clathrin-dependent endocytosis. Indeed, pretreatment of virus with α_vβ₃ integrin or pretreatment of cells with a monoclonal antibody against α_vβ₃ integrin was found to inhibit SARS-CoV-2 entry into HL-mECs. Surprisingly, the anti-Spike antibodies evoked by vaccination were neither able to impair Spike/integrin interaction nor to prevent SARS-CoV-2 entry into HL-mECs. Our data highlight the RGD motif in the Spike protein as a functional constraint aimed to maintain the interaction of the viral envelope with integrins. At the same time, our evidences call for the need of intervention strategies aimed to neutralize the SARS-CoV-2 integrin-mediated infection of ACE2-negative cells in the vaccine era.     

Reinforced 3D Composite Structures of γ-, α-Al2O3 with Carbon Nanotubes and Reduced GO Ribbons Printed from Boehmite Gels

The ability of boehmite to form printable inks has sparked interest in the manufacturing of 3D alumina (Al₂O₃) and composite structures by enabling direct ink writing methods while avoiding the use of printing additives. These materials may exhibit high porosity due to the printing and sintering procedures, depending on the intended application. The 3D-printed porous composite structures of γ-Al₂O₃ and α-Al₂O₃ containing 2 wt.% of carbon nanotubes or reduced graphene oxide ribbons were fabricated from boehmite gels, followed by different heat treatments. The reinforcing effect of these carbon nanostructures was evidenced by compression tests carried out on the different alumina structures. A maximum relative increase of 50% in compressive strength was achieved for the γ-Al₂O₃ composite structure reinforced with reduced graphene oxide ribbons, which was also accompanied by an increase in the specific surface area.     

Inhalation of α1-Protease Inhibitor in Cystic Fibrosis does not affect Surfactant Convertase and Surface Activity

The inhalation of alpha(1)-protease inhibitor (alpha(1)-PI) was assessed in a pilot study to restore the protease-antiprotease balance in the lungs of cystic fibrosis (CF) patients. In addition, the effect of this treatment on the surface active properties of lung surfactant and the metabolic conversion of aggregate forms was studied. Eight young adults with CF inhaled 100 mg of alpha(1)-PI twice daily over 8 weeks and bronchoalveolar lavages (BAL) were obtained before and 12 h after the last inhalation. Large aggregate (LA) forms of surfactant were isolated from the in vivo material by ultracentrifugation and their conversion into small aggregates (SA) was assessed by an in vitro surface area cycling assay. Although alpha(1)-PI partially restored the protease-anti-protease imbalance and reduced BAL protein content, no effects were noted on the impaired minimal surface tension and on the in vivo and in vitro conversion of LA to SA. Antiserum against the specific carboxyl esterase ES-2, previously identified in mice and rats as the putative surfactant convertase, did not detect a protein of the appropriate size in CF BAL. Whereas short-term inhalation of alpha(1)-PI was beneficial for the proteolytic aspects of CF lung injury, this appeared not to be the case for surfactant conversion and surface activity. Copyright Academic Press.     

δβ -Thalassaemia in Two Yugoslavian Families

Members of two Yugoslavian families were found to have δβ-thalassaemia. Interaction of β-thalassaemia with δβ-thalassaemia occurred in two young children producing a clinical condition which is somewhat less severe than that of homozygous β-thalassaemia. Results from biosynthetic analyses indicate that the degree of globin chain imbalance in double heterozygotes for β- and δβ-thalassaemia is similar to that in homozygous β-thalassaemia. Fetal haemoglobin of all heterozygotes contained ^Gγ and ^Aγ chains in an average ratio of about 2:3 whereas that in the two double heterozygotes had ^Gγ and ^Aγ chains in a ratio of 3:2.     

Autocrine Regulation of TGF β Expression in Adult Cardiomyocytes

G. Taimor, K.-D. Schlüter, K. Frischkopf, M. Flesch, S. Rosenkranz and H. M. Piper. Autocrine Regulation of TGF β Expression in Adult Cardiomyocytes. Journal of Molecular and Cellular Cardiology (1999)31 , 2127–2136. As shown before, TGF β acts in an autocrine manner on the induction of hypertrophic responsiveness to β -adrenoceptor stimulation in cultured ventricular cardiomyocytes of adult rat. We now investigated how TGF β expression and activation is regulated in these cultures and how β -adrenoceptor stimulation influences TGF β -mRNA expression. It was found that freshly isolated cardiomyocytes secrete latent TGF β in the culture medium. Supplementation of the cultures with 20% FCS resulted in activation of the secreted TGFβ to 4.1±0.2 ng/ml active TGF β after 6 days. Presence of the protease inhibitor aprotinin (50μ g/ml) reduced TGF β activity by 44±5% (n=5, P<0.05). In cultures supplemented with 5% FCS, TGF β was not activated. Active TGF β downregulated its mRNA-expression: after 6 days TGF β₁-mRNA was reduced to 55.1±11.0%, TGFβ₂ -mRNA to 30.1±16.5%, and TGF β₃-mRNA to 0.3±0.4% in 20% FCS-cultures as compared to their expression in freshly isolated cells (n=4, P<0.05). TGFβ -mRNA expression did not change in cultures without active TGF β. Isoprenaline (1 μ m) increased TGF β₁-mRNA only in cultures which had been pre-exposed to active TGF β. This effect was also seen when hearts from normal mice were compared with hearts from transgenic mice overexpressing TGFβ₁ : only in hearts from transgenic animals perfusion with isoprenaline increased TGFβ₁ -mRNA. In conclusion, isolated cardiomyocytes release latent TGF β, which is activated by external proteases. Active TGF β downregulates its own mRNA expression. Preexposure to TGF β is necessary for a β -adrenoceptor-mediated increase in TGF β₁-mRNA in cardiomyocytes.     

Identification and characterization of an atypical Gαs-biased β2AR agonist that fails to evoke airway smooth muscle cell tachyphylaxis

G protein–coupled receptors display multifunctional signaling, offering the potential for agonist structures to promote conformational selectivity for biased outputs. For β₂-adrenergic receptors (β₂AR), unbiased agonists stabilize conformation(s) that evoke coupling to Gαs (cyclic adenosine monophosphate [cAMP] production/human airway smooth muscle [HASM] cell relaxation) and β-arrestin engagement, the latter acting to quench Gαs signaling, contributing to receptor desensitization/tachyphylaxis. We screened a 40-million-compound scaffold ranking library, revealing unanticipated agonists with dihydroimidazolyl-butyl-cyclic urea scaffolds. The S-stereoisomer of compound C1 shows no detectable β-arrestin engagement/signaling by four methods. However, C1-S retained Gαs signaling—a divergence of the outputs favorable for treating asthma. Functional studies with two models confirmed the biasing: β₂AR-mediated cAMP signaling underwent desensitization to the unbiased agonist albuterol but not to C1-S, and desensitization of HASM cell relaxation was observed with albuterol but not with C1-S. These HASM results indicate biologically pertinent biasing of C1-S, in the context of the relevant physiologic response, in the human cell type of interest. Thus, C1-S was apparently strongly biased away from β-arrestin, in contrast to albuterol and C5-S. C1-S structural modeling and simulations revealed binding differences compared with unbiased epinephrine at transmembrane (TM) segments 3,5,6,7 and ECL2. C1-S (R2 = cyclohexane) was repositioned in the pocket such that it lost a TM6 interaction and gained a TM7 interaction compared with the analogous unbiased C5-S (R2 = benzene group), which appears to contribute to C1-S biasing away from β-arrestin. Thus, an agnostic large chemical-space library identified agonists with receptor interactions that resulted in relevant signal splitting of β₂AR actions favorable for treating obstructive lung disease.

Most G protein–coupled receptors (GPCRs) are now recognized as multisignal transducers (1, 2). Early concepts of agonist–receptor interactions were based on the idea that there was a single “active” receptor conformation induced by the binding of any agonist, resulting in an interaction with the heterotrimeric G protein and a universal, singular signal. Generally, the α-subunit of the G protein, upon its dissociation, was considered the primary activator (or inhibitor) of the effector, resulting in the intracellular signal. Subsequently, it became clear that multiple signaling outcomes from activation of a given GPCR can occur from a single agonist due to specific molecular determinants of the receptor triggering independent mechanisms (3–5). As these multiple functions were being identified, it was apparent that agonists with different structures could act at a given receptor to preferentially activate one signal with minimal engagement of others, a property later termed signal biasing (6–8). Biased agonists, then, could represent important advantages over nonbiased agonists due to this signal selectivity, activating a specified therapeutic pathway while minimally evoking unnecessary or deleterious signaling. The pathway selectivity of biased agonists is thought to be established by the stabilization of specific conformation(s) of the agonist–receptor complex via a set of interactions that differ from those of unbiased (also called balanced) agonists (9–12). While it is conceivable that small modifications of established cognate agonists might yield such specialized signaling, significant deviation from common agonist structures may be necessary to meet this goal (13).The signals/functions of a given GPCR that might be sought for selective activation are defined by the cell type, disease, and desired final physiologic function. In asthma and chronic obstructive pulmonary disease (COPD), active human airway smooth muscle (HASM) cellular contraction limits airflow, representing a major cause of morbidity and mortality. β₂-adrenergic receptors (β₂ARs) expressed on HASM cells are the targets for binding of therapeutically administered β-agonists, which relax the cells via a cyclic adenosine monophosphate–mediated mechanism (14). β-agonists are used for treating acute bronchospasm as well as for long-term prevention. However, the HASM bronchodilator response to acute β-agonist is attenuated by receptor desensitization (15), with typical treatments of humans, or isolated HASM cells, leading to a loss of receptor function over time (16–18), clinically termed tachyphylaxis.Agonist-promoted desensitization of β₂AR (and other GPCRs) is due to partial uncoupling of the receptor to the G protein, which is initiated by phosphorylation of intracellular Ser/Thr residues of the receptor by G protein–coupled receptor kinases (GRKs) (19, 20). The GRK-phosphorylated β₂AR recruits β-arrestin1 or β-arrestin2 to these receptors, with subsequent interactions that appear to compete with the receptor for its binding to the Gα subunit, thus attenuating the intracellular response (11, 21). Such competition has been strongly inferred for the β₂AR (22, 23) and is compelling for rhodopsin–arrestin interactions (24). In addition, β-arrestin binding to GPCRs can initiate receptor internalization and other events such as receptor activation of ERK1/2 (25) through its multiprotein adapter functions. Thus β-arrestin engagement can be considered an early “second signal” of the β₂AR as well as a desensitization initiator for attenuating the Gs signal. An agonist that is biased toward Gαs coupling (cAMP production and airway smooth muscle [ASM] relaxation) and away from β-arrestin binding (desensitization) would be desirable in treating obstructive lung diseases, since efficacy would not be attenuated acutely, nor would tachyphylaxis be experienced from extended treatment. While biased agonists favoring either G protein or β-arrestin (6) signaling have been described for some GPCRs (such as μ-opioid and type 1 angiotensin II receptors), Gαs biasing has not been apparent from most studies with catecholamine-like compounds for the β₂AR. Thus, we have little information as to whether the two β₂AR pathways can be differentially activated in a selective manner by an efficacious agonist, nor is it apparent from a structural standpoint what strategy might be employed to design agonists biased in this manner for this receptor.In order to find this type of biasing for the β₂AR, we screened a 40-million-compound scaffold ranking (SR) library that was agnostic to known β₂AR agonist structures. We found a scaffold in which substitutions of certain R groups led to individual compounds that are apparently Gαs-biased agonists for β₂AR with no apparent engagement of β-arrestin in model systems. Additional studies in HASM cells revealed a lack of tachyphylaxis of the relaxation effect by the lead compound compared with the most widely utilized β₂AR agonist, albuterol. The structure of this biased agonist is very different from that of catecholamine-like agonists. To ascertain the mechanism that may underlie this biased activity, we used structural modeling and molecular simulations and studied homologous compounds with different R groups and receptor mutagenesis to predict the interaction sites with the activated β₂AR. Such studies uncovered distinct structural characteristics that may be responsible for the biasing effect.     

Interaction of heterozygous βo-thalassemia with single functional α-globin gene

In this study, we analyzed the phenotypic manifestations resulting from the interaction of heterozygous β^o-thalassemia(β^o-39 nonsense mutation) with the functional loss of three α-globin structural genes in six subjects, of whom four had the [-αl–] α-globin genotype and two the [–/αThα] α-globin genotype. The β-thalassemia defect was in all cases the nonsense mutation at codon 39. The nondeletion α-thalassemia α^th was the initiation codon mutation (AUG→GUG) of the α-2 gene. In all these subjects hypochromia and microcytosis were more marked than in βα -thalassemia heterozygotes with a full complement of four α-globin genes. All but one had moderate anemia. The α:β globin chain synthesis ratios were consistently decreased. No cases had Hb H on electrophoresis. Subjects with [–/αThα] α-globin genotype had more severe thalassemia-like manifestations than those with [–/-α] α-globin genotype.     

An Individual with Hb-Lepore-Baltimore- δβ-Thalassaemia in a Yugoslavian Family

The clinical, haematological and biochemical findings in a person with δβ-thalassaemia and Hb-Lepore are described. The patient was a 24-year-old student who suffered from anaemia of intermediate seventy with late onset of the clinical manifestations, had minor bone and facial deformities, but had no necessity for regular transfusions. Haemoglobins A and A₂ were absent in this individual, and the Hb-Lepore has been identified as Lepore-Baltimore. Heterogeneity of γ chain of the Hb-F follows the expected pattern. The study provides further evidence that neither β nor δ chains are synthesized in cis to δβ-thalassaemia or Hb-Lepore.     

Crystallographic Calculations and First-Principles Calculations of Heterogeneous Nucleation Potency of γ-Fe on La2O2S Particles

Rare earth (RE) inclusions with high melting points as heterogeneous nucleation in liquid steel have stimulated many recent studies. Evaluating the potency of RE inclusions as heterogeneous nucleation sites of the primary phase is still a challenge. In this work, the edge-to-edge matching (E2EM) model was employed to calculate the atomic matching mismatch and predict the orientation relationship between La₂O₂S and γ-Fe from a crystallographic point of view. A rough orientation relationship (OR) was predicted with the minimum values of fr=9.43% and fd=20.72% as follows: [21¯1¯0]La2O2S∥[100]γ-Fe and (0003¯)La2O2S∥(002¯)γ-Fe. The interface energy and bonding characteristics between La₂O₂S and γ-Fe were calculated on the atomic scale based on a crystallographic study using the first-principles calculation method. The calculations of the interface energy showed that the S-terminated and La(S)-terminated interface structures were more stable. The results of difference charge density, electron localization function (ELF), the Bader charges and the partial density of states (PDOS) study indicated that the La(S)-terminated interface possessed metallic bonds and ionic bonds, and the S-terminated interface exhibited metallic bond and covalent bond characteristics. This work addressed the stability and the characteristics of the La₂O₂S/γ-Fe interface structure from the standpoint of crystallography and energetics, which provides an effective theoretical support to the study the heterogeneous nucleation mechanism. As a result, La₂O₂S particles are not an effective heterogeneous nucleation site for the γ-Fe matrix from crystallography and energetics points of view.     

Gamma-chain heterogeneity in Greek (δβ)O-thalassemia.

Abstract: A molecular and biochemical population study of (δβ)^O thalassemia in central Greece is described. The molecular study was focused on the type of the deletion and the status of ^Gγ-Xmn***l polymorphism, whereas the biochemical approach was centered on the ^Gγ/^Aγ ratio as well as the frequency of the ^Aγ ^T chain in the fetal hemoglobin of 19 δβ-thalassemia heterozygotes and 3 homozygotes. This study includes individuals from the mountainous district of Epirus (northwestern Greece) where the trait was found to be concentrated along the river Arachthos. The Sicilian (δβ)^O thalassemia deletion was found in all subjects tested by direct PCR. The levels for the ^Gγ-chain presented values ranging from 29 to 83% of the total γ -chain content. Thirteen heterozygotes had the adult ^Gγ /^Aγ ratio (mean ^Gγ: 35% ± 10) of whom 10 were Xmnl-negative (-/-), 6 had the newborn ratio (mean ^Gγ: 70% ± 9) and were Xmnl-positive, while homozygotes had equal amounts of ^Gγ and ^Aγ. Five of the 19 heterozygotes were ^Aγ ^T-positive with low levels of this ^Aγ-chain variant, suggesting an in-trans to the δβ-thalassemia determinant production.     

Peculiarities of γ-Al2O3 Crystallization on the Surface of h-BN Particles

The main goal of the present work was to synthesize a composite consisting of h-BN particles coated with a γ-Al₂O₃ nanolayer. A method was proposed for applying nanocrystalline γ-Al₂O₃ to h-BN particles using a sol–gel technique, which ensures the chemical homogeneity of the composite at the nano level. It has been determined that during crystallization on the h-BN surface, the proportion of spinel in alumina decreases from 40 wt.% in pure γ-Al₂O₃ to 30 wt.% as a result of the involvement of the B³⁺ ions from the surface nitride monolayers into the transition complex. For comparison, nano-alumina was synthesized from the same sol under the same conditions as the composite. The characterization of the obtained nanostructured powders was carried out using TEM and XRD. A mechanism is proposed for the formation of a nanostructured γ-Al₂O₃@h-BN composite during the interaction of Al-containing sol and h-BN suspension in aqueous organic media. The resulting composite is a promising model of powdered raw materials for the development of fine-grained ceramic materials for a wide range of applications.     

A High-Performance ε-Ga2O3-Based Deep-Ultraviolet Photodetector Array for Solar-Blind Imaging

One of the most important applications of photodetectors is as sensing units in imaging systems. In practical applications, a photodetector array with high uniformity and high performance is an indispensable part of the imaging system. Herein, a photodetector array (5 × 4) consisting of 20 photodetector units, in which the photosensitive layer involves preprocessing commercial ε-Ga₂O₃ films with high temperature annealing, have been constructed by low-cost magnetron sputtering and mask processes. The ε-Ga₂O₃ ultraviolet photodetector unit shows excellent responsivity and detectivity of 6.18 A/W and 5 × 10¹³ Jones, respectively, an ultra-high light-to-dark ratio of 1.45 × 10⁵, and a fast photoresponse speed (0.14/0.09 s). At the same time, the device also shows good solar-blind characteristics and stability. Based on this, we demonstrate an ε-Ga₂O₃-thin-film-based solar-blind ultraviolet detector array with high uniformity and high performance for solar-blind imaging in optoelectronic integration applications.     

Development of Calcium Carbonate-Based Coatings by the Carbonation of Gamma-C2S (γ-C2S)

A calcium carbonate (CaCO₃)-based coating with gamma-C₂S (γ-C₂S) as the main carbonatable binder is proposed to protect the metal substrate against corrosion in this paper. Here, the morphology and phase assemblage of the coatings are studied by scanning electron microscopy (SEM) and X-ray diffraction (XRD), and the corrosion resistance of the coating is evaluated by electrochemical impedance spectroscopy (EIS) and X-ray photoelectron spectroscopy (XPS). Results show that the carbonated coating has excellent properties in terms of ultraviolet (UV) aging resistance, salt fog resistance, and electrochemical corrosion resistance. The porosity of deposited coating on steel substrates decreases by 47.1% after carbonation due to the compacted calcium carbonate formation, which is recognized as a self-compacting process during carbonation. The coating also exhibits rapid strength development within the first 2 h of carbonation; both the CO₂ uptake efficiency and degree of carbonation (DOC) can reach more than 95% of the total CO₂ uptake efficiency and final DOC values. This study provides a novel insight to extend the category of inorganic coating with additional benefits of CO₂ solidification.