Interleukin-2 receptor (Tac antigen) expressed on adult T cell leukemia cells.

We studied the expression of the interleukin-2 (IL-2) receptor and the proliferative response to exogenous IL-2 of peripheral blood leukemic cells from patients with adult T cell leukemia (ATL) in order to see whether IL-2 receptor expressed on ATL cells is different from normal IL-2 receptor and whether it plays a role in the neoplastic growth in ATL. Peripheral blood leukemic cells from 42 patients with ATL examined expressed IL-2 receptors that were detected by anti-Tac monoclonal antibody when examined immediately after the separation of cells or after the culture for 24 or 48 h. The number of anti-Tac binding sites ranged from 3,100 to 11,400 in fresh cells and from 3,600 to 96,000/cell in short-term cultured leukemic cells, whereas phytohemagglutinin-P (PHA-P)-stimulated normal T cells exhibited 6,900-35,000 anti-Tac binding sites per cell. ATL-derived and human T cell leukemia/lymphoma virus, type I (HTLV-I)-infected cell lines such as MT-1 and Hut102 expressed a much higher number of anti-Tac binding sites. Leukemic cells from 15 patients with ATL examined showed no or very poor proliferative response to various concentrations of immunoaffinity-purified IL-2, although they expressed Tac antigen (Ag). Radiolabeled IL-2 binding experiments demonstrated that ATL leukemic cells could bind IL-2, and they expressed both high and low affinity IL-2 receptors, although the number of high affinity IL-2 receptor was much less than that of low affinity IL-2 receptor and that of anti-Tac binding sites. In contrast, leukemic T cells from a patient with T cell chronic lymphocytic leukemia (CLL), in whom HTLV-I infection was not demonstrated, responded as well as PHA-P-stimulated normal T cells, and their IL-2 receptors, unlike ATL cells, were modulated (down regulated) by anti-Tac antibody. No differences were noted between ATL cells and normal activated T cells in one-dimensional sodium dodecyl sulfate polyacrylamide gel electrophoresis analysis of the IL-2 receptor. Thus, leukemic cells in ATL spontaneously and continuously express IL-2 receptor, which appears to be abnormally regulated and unresponsive to IL-2. These results, taken together with those on normal IL-2 receptors on HTLV-I-negative T-CLL cells, suggest that abnormal expression of the IL-2 receptor in ATL is closely associated with HTLV-I infection and may play a role in the neoplastic growth of ATL cells.     

Interleukin 2 regulates the expression of Tac antigen on peripheral blood T lymphocytes

We investigated the effect of OKT3 antibody and interleukin 2 (IL-2) on Tac antigen expression and the proliferation of human peripheral blood mononuclear leukocytes. OKT3 monoclonal antibody at low, nonmitogenic concentrations (25 pg/ml) or IL-2 alone at optimal concentrations (20 U/ml) did not induce IL-2 receptor expression, as measured by Tac antibody or by T cell proliferation. However, costimulation with these concentrations of OKT3 antibody and IL-2 led to Tac antigen expression and T cell proliferation. These data suggest that the T cells are activated in two steps: OKT3 antibody at 25 pg/ml does not induce Tac antigen expression, but preactivates T cells to become responsive to IL-2. The addition of exogenous IL-2 then leads to expression of the IL-2 receptor, as recognized by Tac antibody, and to subsequent proliferation.     

Direct T helper-B cell interactions induce an early B cell activation antigen

We have explored the consequences for the B cell of cognate interaction with T cells. Early expression of the B cell-restricted cell surface activation antigen, BLAST-2, has been used as an assay system to measure direct T-B cell collaboration. BLAST-2 is preferentially expressed by allogenic B cells cultured with MHC class II antigen-restricted Th clone cells matched to the DR specificity of the target B cells. B cells cultured with DR-mismatched allospecific Th cells express minimal BLAST-2. Th cell-induced BLAST-2 expression appears to be accessory cell independent and occurs as early as 8 h after initiation of culture, with peak expression at 18 h. Direct T-B cell contact, rather than Th-derived lymphokines, provides the most efficient stimulus for BLAST-2 expression. Crosslinking of sIg on B cells is a poor stimulus for BLAST-2 expression. The BLAST-2 assay permits the evaluation of early events associated with B cell activation through cognate interactions, and may facilitate subsequent studies of the mechanism of B cell differentiation.     

血浆转化生长因子结合蛋白2联合鳞状细胞癌抗原检测在肺癌诊断中的应用价值

目的 探讨血浆转化生长因子结合蛋白2(LTBP2)联合鳞状细胞癌抗原(SCC)检测在肺癌诊断中的应用价值.方法 将2019年1月至2021年1月该院收治的原发性肺癌患者104例纳入研究作为肺癌组,另选取50例肺炎患者作为肺炎组,100例体检健康者作为健康对照组.采集上述人群血液标本,应用酶联免疫吸附试验(ELISA)和全自动化学发光仪分别检测血清LTBP2和SCC水平.分析血清LTBP2水平与肺癌患者临床特征的关系.采用受试者工作特征(ROC)曲线分析血清LTBP2和SCC水平检测用于肺癌诊断的价值.结果 肺癌组血清LTBP2及SCC水平均高于肺炎组和健康对照组(P<0.05).TNM分期Ⅲ～Ⅳ期、有淋巴结转移、深层浸润的肺癌患者血清LTBP2水平较高(P<0.05).血清LTBP2水平检测用于诊断肺癌的曲线下面积(AUC)为0.842(95％CI:0.704～0.916),灵敏度为89.15％,特异度为83.94％;血清SCC用于肺癌诊断的AUC为0.794(95％CI:0.529～0.843),灵敏度为82.17％,特异度为70.63％.血清LTBP2和SCC联合检测用于肺癌诊断的AUC为0.887(95％CI:0.752～0.974),灵敏度为92.67％,特异度为86.63％.结论 原发性肺癌患者血清LTBP2水平升高,可能与肺癌的发生及进展有关,LTBP2联合SCC检测更利于临床肺癌的鉴别诊断.     

Antigen valence determines the binding of nominal antigen to cytolytic T cell clones

We have shown that cytotoxic T cell clones specific for the nominal antigen FL will bind high molecular weight (600,000 to 2,000,000) polyacrylamide and Ficoll polymers conjugated with 200-600 FL groups per molecule. Low molecular weight polymers (40,000) with the same epitope density did not give stable binding. A high molecular weight polymer with a lower epitope density also failed to bind. Taken together, these results suggest that a substantial degree of multivalence is a necessary factor in the stable binding of nominal antigen to T cell clones.     

T cell growth factor abrogates concanavalin A-induced suppressor cell function

Concanavalin A (Con-A)-induced suppressor T cells were found to respond to T cell growth factor (TCGF) by proliferation. TCGF abrogated the suppressor activity exerted by these cells on phytohemagglutinin (PHA)- and alloantigen- induced lymphocyte proliferation and on pokeweed mitogen (PWM)-driven immunoglobulin secretion. The Con-A-activated suppressor T cells absorbed the TCGF activity, preincubation of these active suppressor cells with TCGF abolished their suppressor activity and addition of increasing numbers of Con-A-activated T cells reverted the abrogator,/ effect of TCGF. Altogether, these findings suggest that Con-A-induced suppressor T cells exert their function by decreasing the available levels of TCGF. Cyclosporin-A (CYA), which is known to inhibit the expression of receptors for TCGF on T cells, also inhibited the suppressor activity as determined in both indicator systems, namely PHA- or alloantigen-induced DNA synthesis and PWM-induced immunoglobulin synthesis. CYA made Con-A-treated T cells unresponsive to TCGF and unable to absorb the growth factor, supporting the notion that CYA inhibits the expression of TCGF receptors on T cells, a mechanism by which this drug seems to abrogate Con-A-induced suppressor T cell function.     

Functional analysis of the antigen binding site on the T cell receptor alpha chain

We have identified residues on a T cell receptor (TCR) alpha chain that are important for interaction with antigen/major histocompatibility complex (MHC). Using site-directed mutagenesis, we modified DNA encoding the postulated antigen/MHC binding loops on the TCR alpha chain expressed by the T cell clone D5, which recognizes p-azobenzenearsonate-conjugated antigens presented by cells bearing I-Ad. These variant TCR alpha chains were expressed in conjunction with the wild-type D5 TCR beta chain on the surface of hybridoma cells, and were tested for the ability to recognize hapten-conjugated antigens presented by I-Ad. Individual amino acid substitutions in each of the three antigen binding loops (alpha 1, alpha 2, alpha 3) of the D5 TCR alpha chain affected antigen recognition, demonstrating that all three loops are important in recognition of antigen/MHC. A subset of the single amino acid substitutions completely eliminated antigen recognition, thus identifying the residues that are particularly important in the recognition of antigenic peptide/MHC by the D5 TCR. Because the wild-type D5 TCR recognizes arsonate and certain structural analogues of arsonate conjugated to a variety of protein antigens, we were able to test whether the TCR substitutions affected the specificity of the D5 TCR for hapten or carrier antigen. One substitution introduced into antigen binding loop alpha 3 markedly altered the pattern of carrier recognition. Together, these results verify the Ig model for the TCR and are consistent with the proposition that residues forming the first and second antigen binding loops of the TCR contact the MHC, while those forming the third loop contact mainly antigenic peptides.     

Human cutaneous T cell lymphoma and leukemia cell lines produce and respond to T cell growth factor

Three cell lines of mature T cell origin derived from patients with cutaneous T cell lymphoma-leukemias (CTCL) were found to be constitutive producers of T cell growth factor (L-TCGF). These are the first reported human cell lines which constitutively produce TCGF. Biologically active TCGF could also be eluted from the surface of these cells using an acid glycine buffer under conditions that maintained cell viability, and subcellular fractionation showed that almost all the TCGF activity was associated with the plasma membrane. Over 30 other human hematopoietic cell lines derived from other disorders were unable to produce TCGF even after induction, and their acid eluates did not contain TCGF activity. L-TCGF from CTCL lines had the same biological activity as TCGF obtained from normal leukocytes (N-TCGF) in that they both supported the long-term growth of normal T cells only after the cells were previously activated by antigen or lectin. Both L-TCGF and N-TCGF increased the rate of proliferation of TCGF-independent and TCGF-dependent CTCL cell lines. The same three factor-independent cell lines that released TCGF adsorbed TCGF in a cell-concentration, time-, and temperature-dependent manner. Since the CTCL cell lines produce TCGF, adsorb TCGF, and increase their proliferative rate in response to TCGF or a related molecule, it is suggested that this endogenously produced factor plays a role in maintaining the abnormal proliferation of these cells in culture as permanently growing cell lines independent of exogenous TCGF. However, this does not mean that this is an essential aspect of neoplastic transformation. Since it is unusual to develop these cell lines in the absence of the continuous need for added TCGF, “autostimulation” may be one of the many unusual variant phenotypic properties sometimes associated with neoplastic cells that gives them a selective advantage for in vitro growth.     

Dominant-negative zeta-associated protein 70 inhibits T cell antigen receptor signaling

Zeta-associated protein (ZAP)-70 is a cytoplasmic protein tyrosine required for T cell antigen receptor (TCR) signaling and development. Mutations in ZAP-70 result in severe combined immunodeficiency in humans. ZAP-70 interacts with the TCR by binding to tyrosine- phosphorylated immunoreceptor tyrosine-based activation motifs (ITAMs) present in the invariant subunits of the TCR complex. Here we report that two ZAP-70 mutants devoid of kinase activity, generated either by a point mutation in the kinase domain to create an inactive kinase, or by truncation of the entire kinase domain (SH2[N+C]), functioned as dominant-negative mutants to specifically suppress TCR-mediated activation of NFAT, a nuclear factor essential for inducible interleukin 2 gene expression. Biochemical studies with the SH2(N+C) mutant showed that it also blocked early TCR signaling events, such as p95vav tyrosine phosphorylation, extracellular signal-regulated kinase 2 activation, and the association of a number of tyrosine- phosphorylated proteins with growth factor receptor-binding protein 2 (GRB2). The inhibitory effects of the SH2(N+C) mutant revealed that it requires an intact phosphotyrosine-binding site in its COOH-terminal SH2 domain. Using a CD8-zeta chimeric receptor to analyze the interaction of the SH2(N+C) mutant with ITAMs of TCR-zeta, we found that this mutant was constitutively bound to the hyperphosphorylated CD8-zeta chimera. These results indicate that tyrosine-phosphorylated ITAM is the target for the action of this dominant-negative mutant, suggesting that the assembly of a functional receptor signaling complex on ITAMs is a critical proximal TCR signaling event leading to downstream activation.     

Radioimmunoassay of growth hormone-dependent insulinlike growth factor binding protein in human plasma.

A specific radioimmunoassay has been established for a growth hormone-dependent insulinlike growth factor (IGF) binding protein (BP) from human plasma. Although the assay was directed against a 53-kD, acid-stable BP subunit, the main immunoreactive BP in the circulation had an apparent molecular mass of approximately 125 kD. Only higher primate species showed cross-reactivity, and IGF-I, IGF-II, and other peptides were without effect. Circulating BP levels in healthy subjects rose threefold from early childhood to puberty. In 65 adults aged 18 to 65, the mean level (+/- SD) was 6.12 +/- 1.43 micrograms/ml, and declined with age. Strong growth hormone-dependence of BP was also seen; there was a 2.2-fold increase in active acromegaly and a 50-80% reduction in growth hormone deficiency. Poorly controlled diabetic subjects had BP levels 40% below normal, whereas in renal failure and third-term pregnancy a mild elevation was seen. Measurement of BP may provide a useful adjunct to IGF assays in growth disorders.     

Quantifying in vivo murine antigen-specific T cell responses without requirement for prior knowledge of antigen identity

Extracorporeal Photochemotherapy (ECP) is a widely applied anti-cancer immunotherapy for patients with cutaneous T cell lymphoma (CTCL). By using apoptotic malignant cells as a source of patient-specific tumor antigen, it enables clinically relevant and curative anti-CTCL immunity, with potential efficacy in other tumors. Currentmethods to track patient-specific responses are tedious, and new methods are needed to assess putative global immunity. We developed a clinically practical method to assess antigen-specific T cell activation that does not rely on knowledge of the particular antigen, thereby eliminating the requirement for patient-specific reagents. In the OT-I transgenic murine system, we quantified calcium flux to reveal early T cell engagement by antigen presenting cells constitutively displaying a model antigenic peptide, ovalbumin (OVA)-derived SIINFEKL. We detected calcium flux in OVA-specific T cells, triggered by specific T cell receptor engagement by SIINFEKL peptide-loaded DC. This approach led to sensitive detection of antigen-specific calcium flux (ACF) down to a peptide-loading concentration of ～10^?3 uM and at a frequency of ～0.1% OT-I cells among wild-type (WT), non-responding cells. Antigen-specific T cells were detected in spleen, lymph nodes, and peripheral blood after adoptive transfer into control recipient mice. Methods like this for assessing therapeutic response are lacking in patients currently on immune-based therapies, such as ECP, where assessment of clinical response is made by delayed measurement of the size of the malignant clone. These findings suggest an early, practical way to measure therapeutically-induced anti-tumor responses in ECP-treated patients that have been immunized against their malignant cells.     

Cell growth cycle block of T cell hybridomas upon activation with antigen

Stimulation of antigen-specific T cell hybridomas with the appropriate antigen/MHC combination, at concentrations that resulted in the secretion of the lymphokine interleukin 2, resulted in a dose-dependent decrease in both [3H]thymidine incorporation and cell growth. Flow cytometric studies demonstrated that stimulation with antigen resulted in a cell cycle block that was most evident at the G1/S border, and mixing studies revealed that bystander T cells of different antigen specificities were not affected. For at least the large majority of T cells, the G1/S cell cycle block appeared to be irreversible after 24 h of exposure to antigen. This cell cycle block may be useful as a rapid and quantitative measure of T cell hybridoma activation, as a means of selecting T cell hybridomas that have functional alterations in the reception of stimulatory signals, and may serve as a model of the induction of tolerance in immature T cells.     

T suppressor cell growth factor and anti-CD3 antibodies stimulate reciprocal subsets of T lymphocytes

Because of the central role of IL-2 in clonal expansion of T cells, we have postulated that lymphocyte subpopulations with opposing regulatory functions might be independently regulated by differential requirements for expression of cell-surface IL-2-R. Purified CD4+ and CD8+ cells proliferated in an IL-2-dependent manner to crosslinked anti-T cell receptor antibodies (anti-CD3-Seph). Similarly, both CD4+ and CD8+ cells became IL-2 responsive after incubation in T suppressor cell growth factor (TsGF), a newly described approximately 8,000 Mr product of activated CD4+ cells. In support of our hypothesis, however, we observed that subpopulations of CD4+ and CD8+ cells, possessing distinct cell-surface antigens, showed differential responses to these stimuli. Those cells of suppressor-inducer or suppressor-effector phenotype failed to proliferate when cultured in anti-CD3-Seph plus IL-2, but did proliferate in an IL-2-dependent manner to TsGF. Furthermore, the suppressor-effector population was unresponsive to TsGF plus IL-2 when cocultured in anti-CD3-Seph, suggesting that functionally induced Ts may be refractory to growth stimuli. Conversely, cells with helper-inducer or cytolytic phenotype proliferated when incubated in anti-CD3-Seph and IL-2, while remaining essentially unresponsive to TsGF and IL-2. The results could not be explained by differences in the level of CD3 expression by the T cell subsets. Thus, cells within the helper and suppressor lineages appear to have distinct and reciprocal patterns for the induction of IL-2 responsiveness.     

A common polymorphism in the human insulin-like growth factor binding protein 3 gene

A common polymorphism generated by an A to C transition at nucleotide 7580 in the third intron of the insulin-like growth factor binding protein 3 gene was found. This polymorphism can be identified by Nde 1 restriction of genomic DNA amplified with a specifically designed restriction enzyme site-generating oligonucleotide primer. The frequency of the A and C alleles was estimated at 0.6 and 0.4 in the Caucasians, 0.63 and 0.37 in Blacks, respectively.     

Production of transforming growth factor beta by human T lymphocytes and its potential role in the regulation of T cell growth

This study examines the potential role of transforming growth factor beta (TGF-beta) in the regulation of human T lymphocyte proliferation, and proposes that TGF-beta is an important autoregulatory lymphokine that limits T lymphocyte clonal expansion, and that TGF-beta production by T lymphocytes is important in T cell interactions with other cell types. TGF-beta was shown to inhibit IL-2-dependent T cell proliferation. The addition of picograms amounts of TGF-beta to cultures of IL-2-stimulated human T lymphocytes suppressed DNA synthesis by 60-80%. A potential mechanism of this inhibition was found. TGF-beta inhibited IL-2-induced upregulation of the IL-2 and transferrin receptors. Specific high-affinity receptors for TGF-beta were found both on resting and activated T cells. Cellular activation was shown to result in a five- to sixfold increase in the number of TGF-beta receptors on a per cell basis, without a change in the affinity of the receptor. Finally, the observations that activated T cells produce TGF-beta mRNA and that TGF-beta biologic activity is present in supernatants conditioned by activated T cells is strong evidence that T cells themselves are a source of TGF-beta. Resting T cells were found to have low to undetectable levels of TGF-beta mRNA, while PHA activation resulted in a rapid increase in TGF-beta mRNA levels (within 2 h). Both T4 and T8 lymphocytes were found to make mRNA for TGF-beta upon activation. Using both a soft agar assay and a competitive binding assay, TGF-beta biologic activity was found in supernatants conditioned by T cells; T cell activation resulted in a 10-50-fold increase in TGF-beta production. Thus, TGF-beta may be an important antigen-nonspecific regulator of human T cell proliferation, and important in T cell interaction with other cell types whose cellular functions are modulated by TGF-beta.     

Factors regulating macrophage production and growth: identity of colony- stimulating factor and macrophage growth factor

The activities of a colony-stimulating factor (CSF), which stimulates granulocyte-macrophage colony formation by mouse hemopoietic cells, and macrophage growth factor (MGF), which stimulates proliferation of activated peritoneal macrophages, have been demonstrated by various criteria to reside in the same molecular species. These criteria include occurrence in various sources and copurification of the activities in mouse L-cell-conditioned medium as well as the biological, physicochemical, and antigenic properties of the activities of L-cell-conditioned medium. CSF and MGF activities of L-cell-conditioned medium are ascribable to a glycoprotein of mol wt approximately 60,000 which migrates electrophoretically with alpha-globulin. Human urinary CSF, which also possesses MGF activity, has similar properties and can be neutralized by antiserum to highly purified L-cell medium CSF. A procedure is described for the partial purification of material from L-cell medium that has activity at 1 ng/ml in both MGF and CSF assays.     

异常疤痕中血管内皮生长因子和增殖细胞核抗原的表达

目的 探讨瘢痕疙瘩和增殖性瘢痕等异常疤痕中血管作者简介：李军辉 (1970-),男,江西人,整形外科讲师,硕士,研究方向：异常疤痕防治。 内皮生长因子（ VEGF）和增殖细胞核抗原（ PCNA）的表达及其意义。方法 应用免疫组织化学染色技术,以正常皮肤和正常瘢痕作对照,观察了瘢痕疙瘩和增殖性瘢痕中 VEGF和 PCNA的表达。结果 瘢痕疙瘩和增殖性瘢痕基底层角朊细胞均大量表达 VEGF,较正常皮肤和正常瘢痕显著增加。 PCNA的表达与 VEGF相似,但真皮内少量的成纤维细胞有较弱的 PCNA表达。结论 瘢痕疙瘩和增殖性瘢痕表皮基底层的角朊细胞大量表达 VEGF和 PCNA可能与异常疤痕的形成密切相关。     

血小板衍生生长因子促进鼠骨早期修复中增殖细胞核抗原与c—Jun蛋白的表达

目的：将重组人血小板衍生生长因子（platelet-derived growth factor AB．PDGF-AB）注入大鼠桡骨骨缺损模型，同体双侧对照，运用免疫组织化学染色方法，从细胞分子水平观察和分析血小板衍生生长因子对骨折愈合期间软骨骨痂发生、生长的刺激作用及其刺激信号的传导机制。 方法：实验于2004—12／2005—08在解放军总医院三○四临床部烧伤研究所完成。①SD大鼠30只，造成双侧上肢平均约3mm的桡骨骨缺损模型。将重组因子PDGF-AB分别于术后第1，3，5，7天分4次注人大鼠右侧桡骨骨缺损区内（血小板衍生生长因子组），左侧骨缺损区内注入生理盐水作为对照组。②两组分别于术后第1，2，4周各取10只大鼠骨痂组织做成切片，分别进行增殖细胞核抗原与c-Jun免疫组织化学观察并对阳性结果作定量分析。 结果：30只大鼠全部进入结果分析。①增殖细胞核抗原蛋白与c-Jun蛋白在软骨骨痂形成与转归中的表达规律有比较一致的相似性，且增殖细胞核抗原能刺激间充质细胞、软骨细胞合成这两种蛋白。②术后1周，血小板衍生生长因子组间充质细胞内增殖细胞核抗原蛋白与c-Jun蛋白表达均高于生理盐水组[（6．07±2．09）×10^-3比（3．78±1．84）×10^-3，（8．62±2．10）×10^-3比（4．89±1．74）×10^-3，P值均小于0．01]。③术后2周，血小板衍生生长因子组非肥大软骨细胞内增殖细胞核抗原蛋白与c-jun蛋白表达均高于生理盐水组（4．33±1．26）×10^-3比（3．05±1．14）×10^-3，P〈0．05；（6．84±1．45）×10^-3比（5．00±1．18）×10^-3。P〈0．01）。 结论：血小板衍生生长因子能刺激动物体内间充质细胞和软骨细胞的增殖，加速软骨骨痂的形成，促进骨愈合。血小板衍生生长因子能诱导这两种细胞表达c-Jun，它或许能通过C—FOS／JUN蛋白来传递其生长作用信号，从而实现其刺?     

血小板衍生生长因子促进鼠骨早期修复中增殖细胞核抗原与c-Jun蛋白的表达

目的:将重组人血小板衍生生长因子(platelet-derivedgrowthfactorAB,PDGF-AB)注入大鼠桡骨骨缺损模型,同体双侧对照,运用免疫组织化学染色方法,从细胞分子水平观察和分析血小板衍生生长因子对骨折愈合期间软骨骨痂发生、生长的刺激作用及其刺激信号的传导机制。方法:实验于2004-12/2005-08在解放军总医院三○四临床部烧伤研究所完成。①SD大鼠30只,造成双侧上肢平均约3mm的桡骨骨缺损模型。将重组因子PDGF-AB分别于术后第1,3,5,7天分4次注入大鼠右侧桡骨骨缺损区内(血小板衍生生长因子组),左侧骨缺损区内注入生理盐水作为对照组。②两组分别于术后第1,2,4周各取10只大鼠骨痂组织做成切片,分别进行增殖细胞核抗原与c-Jun免疫组织化学观察并对阳性结果作定量分析。结果:30只大鼠全部进入结果分析。①增殖细胞核抗原蛋白与c-Jun蛋白在软骨骨痂形成与转归中的表达规律有比较一致的相似性,且增殖细胞核抗原能刺激间充质细胞、软骨细胞合成这两种蛋白。②术后1周,血小板衍生生长因子组间充质细胞内增殖细胞核抗原蛋白与c-Jun蛋白表达均高于生理盐水组[(6.07±2.09)×10-3比(3.78±1.84)×10-3,(8.62±2.10)×10-3比(4.89±1.74)×10-3,P值均小于0.01]。③术后2周,血小板衍生生长因子组非肥大软骨细胞内增殖细胞核抗原蛋白与c-Jun蛋白表达均高于生理盐水组(4.33±1.26)×10-3比(3.05±1.14)×10-3,P<0.05;(6.84±1.45)×10-3比(5.00±1.18)×10-3,P<0.01)。结论:血小板衍生生长因子能刺激动物体内间充质细胞和软骨细胞的增殖,加速软骨骨痂的形成,促进骨愈合。血小板衍生生长因子能诱导这两种细胞表达c-Jun,它或许能通过C-FOS/JUN蛋白来传递其生长作用信号,从而实现其刺激间充质细胞和软骨细胞增殖的目的。