胆囊黏膜ABCA1的表达和胆囊胆固醇息肉发病关系的研究

目的：研究ABCA1在胆囊黏膜的表达及其表达与胆囊胆固醇息肉发病的关系。方法：收集因胆囊疾患而行腹腔镜胆囊切除术病人的胆石、胆汁、胆囊黏膜及胆囊壁全层组织共计42例,其中胆囊胆固醇息肉15例,胆囊胆固醇结石15例,对照组12例（胆囊腺瘤5例,非胆固醇胆囊结石7例）。分别测定胆石胆固醇含量、胆汁胆固醇、胆汁酸、磷脂的浓度;实时PCR定量检测胆囊黏膜ABCA1、LXRα、RXRα的mRNA表达：胆囊壁全层组织做病理切片;免疫组化显示ABCAl蛋白在胆囊黏膜的表达．结果：胆固醇息肉组胆汁胆固醇饱和指数为1．0±0．2,较对照组胆固醇饱和指数0．6±0．3明显增高,其差别有统计学显著性（P〈0．01）。免疫组化显示ABCA1在胆囊黏膜上皮细胞有明显表达。息肉组、结石组和对照组胆囊黏膜ABCAI、LXRa、RXRα mRNA相对表达量比较,各组之间差异无统计学意义。结论：胆囊黏膜ABCA1的表达可能并不是导致胆囊胆固醇息肉发病的重要原因。     

核受体基因在家族遗传性胆囊胆固醇结石患者肝组织中表达的变化

目的:探讨核受体(NRs)基因在汉族人群中家族遗传性胆囊胆固醇结石(HCGD)患者肝组织中表达的变化。方法:收集9例HCGD患者(HCGD组)、9例散发性胆固醇结石患者(SCGD,SCGD组)和7例无胆石病肝血管瘤患者(对照组)血液与手术肝组织标本。用酶法检测血清脂代谢相关指标,用qRT-PCR测定肝组织肝NRs:肝X受体(LXRα)、法尼醇X受体(FXR)、甾醇调节元件结合蛋白2(SREBP2)、雌激素受体α/β(ERα/β)、G蛋白偶联受体30(GPR30)、过氧化物酶体增殖物激活受体γ(PPARγ)mRNA的表达。结果:HCGD组血清总胆汁酸(TBA)含量较对照组与SCGD组明显降低(均P0.05),其余脂代谢相关指标各组间均无统计学差异(均P0.05)。与对照组比较,HCGD组ERα/β、SREBP2、PPARγ的mRNA表达量明显升高,SCGD组FXRmRNA明显升高(均P0.05);LXRα和GPR30mRNA在各组间均无统计学差异(均P0.05)。HCGD组中ERα、ERβmRNA表达与患者血清TBA水平呈负相关(r=-1.000,P=0.000;r=-0.989,P=0.011)。结论:ERα/β、SREBP2、PPARγ基因在HCGD患者肝组织中表达上调,其高表达可能参与了HCGD的发生发展。     

转化生长因子β1在牵张应力刺激促进后纵韧带细胞骨化中的作用

目的研究转化生长因子β1(TGF-β1)在牵张应力刺激促进后纵韧带成纤维细胞骨向分化进程中的作用。方法经颈前路手术获取颈椎后纵韧带骨化症(OPLL)患者的后纵韧带组织,采用组织块培养法进行体外细胞培养及鉴定。通过荧光实时定量PCR检测后纵韧带成纤维细胞在加载牵张应力刺激12 h及24 h后Ⅰ型胶原(COLⅠ)、碱性磷酸酶(ALP)和TGF-β1的mRNA表达变化;并检测在加入外源性TGF-β1或TGF-β1抗体作用后,后纵韧带成纤维细胞在静置或牵张应力刺激下的COLⅠ和ALP的mRNA表达变化。结果 HE及免疫荧光染色证实后纵韧带成纤维细胞培养成功。后纵韧带成纤维细胞经牵张应力刺激12 h及24 h后,细胞COLⅠ、ALP和TGF-β1的mRNA表达与静置相同时间的对照组相比均有升高,且24 h时差异具有统计学意义(P0.05)。加入0.1、1.0、10.0 ng/mL的外源性TGF-β1并静置24 h后细胞COLⅠ及ALP的mRNA表达量升高,其中10.0 ng/mL浓度组与对照组相比差异具有统计学意义(P0.05);而加入2.0μg/mL的TGF-β1抗体并加载牵张应力刺激24 h后细胞的COLⅠ及ALP的mRNA表达量的升高程度与对照组相比明显降低,差异具有统计学意义(P0.05)。结论组织块培养法是进行颈椎OPLL患者后纵韧带成纤维细胞体外培养的有效方法。后纵韧带成纤维细胞在牵张应力刺激下TGF-β1表达上调,且TGF-β1可促进其骨向分化。     

HIV与HBV共感染对肝星状细胞纤维化相关基因表达的影响

目的探讨人类免疫缺陷病毒(HIV)与乙型肝炎病毒(HBV)共感染对人肝星状细胞纤维化部分相关基因表达的影响。方法人肝星状细胞(HSC LX2)分别与HIV X4株(CXCR4噬性)、HIV R5株(CCR5噬性)、HBV、HIV X4+HBV和HIV R5+HBV共同孵育3 d后,采用RTPCR检测细胞中的前胶原蛋白α1(COL1A)、基质金属蛋白酶3(MMP3)及金属蛋白酶组织抑制物1(TIMP1)的mRNA表达水平,采用ELISA检测细胞上悬液中相应蛋白含量,结果分别与相应对照样本进行比较。结果HIV和HBV共同作用于HSC LX2细胞比HIV或HBV单独作用更能促进COL1A蛋白合成(P均0.05)。实验组和对照组中MMP3 mRNA和蛋白表达水平差异虽无统计学意义,但实验数据显示,病毒有抑制MMP3基因表达的趋势。HIV、HBV分别作用于HSC LX2细胞可促进TIMP1mRNA以及TIMP1蛋白表达(P均0.05)。HIV和HBV共同作用能进一步提高TIMP1 mRNA以及TIMP1蛋白表达(P均0.05)。结论HIV、HBV分别作用于HSC LX2细胞,能促进TIMP1 mRNA以及蛋白的表达。HIV、HBV共同作用于HSC LX2细胞比单一病毒更能促进COL1A蛋白的合成以及TIMP1 mRNA转录和蛋白的合成。     

瑞香素联合IGF-1对大鼠脂肪间充质干细胞成软骨分化的影响

目的初步研究瑞香素(dephnetin,DAP)联合IGF-1基因转染对大鼠脂肪间充质干细胞(adiposederived mesenchymal stem cells,ADSCs)成软骨分化的影响。方法采用酶消化法分离培养大鼠ADSCs。取第3代ADSCs以IGF-1基因转染作为实验组,未转染的ADSCs作为对照组。两组细胞分别用不同浓度DAP(0、30、60、90μg/mL)处理,培养72 h后采用细胞计数试剂盒8(cell counting kit 8,CCK-8)法检测细胞增殖活性;培养14 d分别采用实时荧光定量PCR和Western blot检测Ⅱ型胶原和蛋白聚糖(Aggrecan)mRNA和蛋白表达,并行甲苯胺蓝染色及Ⅱ型胶原免疫组织化学染色观察。结果 CCK-8法检测示,随DAP作用浓度增加,对照组和实验组细胞吸光度(A)值均逐渐增加(P0.05);相同DAP浓度下,实验组细胞A值显著高于对照组(P0.05)。实时荧光定量PCR和Western blot检测示,随DAP作用浓度增加,对照组细胞Ⅱ型胶原和Aggrecan的mRNA和蛋白相对表达量无明显变化,各浓度组间差异无统计学意义(P0.05);实验组细胞Ⅱ型胶原和Aggrecan的mRNA和蛋白相对表达量逐渐增加,其中60、90μg/mL DAP浓度组显著高于0μg/mL DAP浓度组(P0.05)。相同DAP浓度下,实验组细胞Ⅱ型胶原和Aggrecan的mRNA和蛋白相对表达量显著高于对照组(P0.05)。甲苯胺蓝染色示,随DAP作用浓度增加,对照组内和实验组内细胞着色无明显差异;相同DAP浓度下,实验组比对照组细胞着色略深。Ⅱ型胶原免疫组织化学染色示,随DAP作用浓度增加,对照组细胞的细胞质内着色无明显差异;实验组细胞的细胞质内着色逐渐加深,其中60、90μg/mL DAP浓度组明显深于0μg/mL DAP浓度组。相同DAP浓度下,实验组比对照组细胞着色明显加深。结论 DAP对大鼠ADSCs增殖有一定促进作用;单独使用DAP诱导大鼠ADSCs向软骨细胞分化作用极微弱,但DAP联合IGF-1基因转染有明显协同作用,促进ADSCs成软骨分化。     

BCAT1对HSC-LX2人肝星状细胞纤维化相关基因表达的影响

[摘要] 目的 探讨支链氨基酸转氨酶1（BCAT1）对HSC-LX2人肝星状细胞纤维化相关基因表达的影响。方法 构建携带BCAT1基因的慢病毒载体,将病毒转染HSC-LX2细胞,运用qRT-PCR和Western blotting检测转染BCAT1过表达病毒后的HSC-LX2细胞中BCAT1、ACTA2、TIMP1、MMP2和COL1A1基因的表达情况。结果 携带BCAT1基因的慢病毒转染HSC-LX2细胞后,实验组（转染p-BCAT1）HSC-LX2细胞和对照组（转染Vec）HSC-LX2细胞相比,促进纤维化的ACTA2、TIMP1、COL1A1基因的mRNA及蛋白表达均升高,抗纤维化的MMP2基因的mRNA及蛋白表达均下降,两者的差异均具有统计学意义（P < 0.05）。结论 BCAT1增强HSC-LX2人肝星状细胞中ACTA2、TIMP1、COL1A1促纤维化相关基因的表达,抑制抗纤维化相关基因MMP2的表达。     

钩藤碱通过Nrf2/HO-1信号通路抑制IL-1β诱导的软骨细胞损伤

目的 探讨钩藤碱对IL-1β诱导的软骨细胞凋亡、氧化应激和炎症等损伤的影响及其分子机制。方法 将大鼠软骨细胞分为对照组、IL-1β(10 ng/mL)组、IL-1β+钩藤碱(5、25、50μmol/L)组;MTT实验检测钩藤碱对细胞活性的影响;Western blot方法检测Bcl2、Bax、MMP3、MMP13、CollagenⅡ、Nrf2和HO-1蛋白水平;ELISA方法检测炎性因子PGE2、COX-1、TNF-α和ROS水平;试剂盒检测MDA水平。结果 与对照组相比,IL-1β组细胞活性明显抑制(P<0.05);与IL-1β组相比,钩藤碱25μmol/L组和50μmol/L组细胞活性增强(P<0.05)。与对照组相比,IL-1β组Bcl2蛋白表达减少,Bax蛋白表达增加(P<0.05);与IL-1β组相比,钩藤碱25μmol/L组和50μmol/L组Bcl2蛋白表达增加,钩藤碱50μmol/L组Bax蛋白表达减少(P<0.05)。与对照组相比,IL-1β组MMP13和MMP3蛋白表达上调,CollagenⅡ蛋白表达下调(P<0.05);与IL-1β组...     

丹参酮ⅡA对人胃癌MKN-45细胞整合素β1、基质金属蛋白酶-7表达影响

目的：通过观察丹参酮ⅡA对胃癌MKN-45细胞的增殖抑制及对整合素β1、基质金属蛋白酶-7（MMP-7）表达的影响,探讨其抗肿瘤机制。方法：MTT法检测不同浓度的丹参酮IIA对体外培养的人胃癌MKN-45细胞增殖的影响 RT-PCR法测丹参酮IIA作用后人胃癌MKN-45细胞整合素β1、MMP-7的表达。结果：与阴性对照组相比,丹参酮ⅡA各浓度组（4μg/mL、8μg/mL、16μg/mL、32μg/mL、64μg/mL）对肿瘤细胞增殖的抑制率有显著差异（P〈0.05）,其24h、48h、72h半数抑制浓度分别为42.5μg/mL、19.4μg/mL和7.4μg/mL。PCR半定量分析表明丹参酮ⅡA作用后整合素β1和MMP-7mRNA的表达受到抑制,抑制程度随着药物浓度的增加而增加。结论：丹参酮ⅡA能有效抑制人胃癌MKN-45细胞的生长,并具有明显的时间和剂量依赖性。丹参酮ⅡA可能通过降低人胃癌MKN-45细胞整合素β1和MMP-7mRNA的表达,而抑制肿瘤细胞增殖。     

胆囊癌GBC-SD细胞经顺铂处理后的survivin表达及意义

目的: 探讨经顺铂（DDP）处理胆囊癌细胞后survivin表达及其与肿瘤细胞耐药之间的关系。 方法:采用MTT比色法测定胆囊癌细胞对4种化疗药物的敏感性。RT-PCR检测survivin mRNA的表达。Western blot检测survivin蛋白表达的变化。结果:GBC-SD细胞对化疗药物的敏感性从高到低依次为DDP>ADM>5-FU>MMC。化学药物处理后的第1天，3组胆囊癌细胞的survivin mRNA表达水平均降低;其中0.5μg/mL DDP＋GBC-SD组下降了10%，3μg /mL DDP＋GBC-SD组下降36%，6μg /mL DDP＋GBC-SD组下降了28%。第3天，0.5μg/mL DDP组和3μg/mL DDP组GBC-SD细胞的survivin mRNA表达与第1天比较，分别上升22%和64%，但6μg/mL DDP组仍持续降低，仅为第1天的66%。0.5μg/mL DDP组和3μg/mL DDP组作用3d后的GBC-SD细胞中survivin蛋白含量分别升高了15%和12%，而6μg/mL DDP组则下降了80%。 结论:低浓度的DDP即能诱导胆囊癌细胞内survivin的表达增加，这可能是胆囊癌细胞对化疗药物产生耐药性的因素之一。     

白细胞介素1β对人肾小球系膜细胞LOX-1和ABCA1表达的影响

目的 研究白细胞介素1β（IL-1β）对人肾小球系膜细胞株（HMCL）植物血凝素样氧化低密度脂蛋白受体1（LOX-1）以及腺苷三磷酸结合盒转运体A1（ABCA1）表达的影响，及其与细胞胆固醇稳态的关系。 方法 实时定量PCR和Western印迹法检测IL-1β对人肾小球系膜细胞LOX-1、ABCA1表达的影响。 结果 人肾小球系膜细胞表达LOX-1 mRNA和蛋白。IL-1β促进人肾小球系膜细胞LOX-1 mRNA和蛋白表达，5 μg/L IL-1β刺激细胞0~24 h，LOX-1 mRNA表达于6 h达高峰，为对照的6.87倍；LOX-1蛋白24 h达高峰，为对照的1.88倍。IL-1β降低脂质负荷的人肾小球系膜细胞 ABCA1 mRNA和蛋白表达。5 μg/L IL-1β刺激细胞0~48 h，48 h时ABCA1 mRNA和蛋白下降最明显，分别为对照的19.0％和50.62％。 结论 IL-1β促进人肾小球系膜细胞LOX-1表达，抑制ABCA1的表达，导致细胞内胆固醇的失衡，促使其变成泡沫细胞，可能加重肾小球硬化和肾病的进展。     

Impaired expression of genes regulating cholesterol efflux in human osteoarthritic chondrocytes

Altered lipid metabolism has been implicated as a critical player in osteoarthritis (OA). Our study aimed to investigate the expression of genes regulating cholesterol efflux in human chondrocytes and to study the effect of an LXR agonist on cholesterol efflux and lipid accumulation in osteoarthritic chondrocytes. ATP‐binding‐cassette transporter A1 (ABCA1), apolipoprotein A1 (ApoA1), and liver X receptors (LXRα and LXRβ) mRNA expression levels were evaluated using real‐time polymerase chain reaction (PCR) and ApoA1 protein levels by Western blot analysis in normal and osteoarthritic articular cartilage samples. Cholesterol efflux was evaluated in osteoarthritic chondrocytes radiolabeled with [1,2(n)‐³H] cholesterol after LXR treatment, while intracellular lipid accumulation was studied after Oil‐red‐O staining. Cholesterol efflux gene expressions were significantly lower in osteoarthritic cartilage compared to normal. Treatment of osteoarthritic chondrocytes with the LXR agonist TO‐901317 significantly increased ApoA1 and ABCA1 expression levels, as well as cholesterol efflux. Additionally, osteoarthritic chondrocytes presented intracellular lipids deposits, while no deposits were found after treatment with TO‐901317. Our findings suggest that impaired expression of genes regulating cholesterol efflux may be a critical player in osteoarthritis, while the ability of the LXR agonist to facilitate cholesterol efflux suggests that it may be a target for therapeutic intervention in osteoarthritis. © 2010 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 28:1033–1039, 2010     

Loss of both ABCA1 and ABCG1 results in increased disturbances in islet sterol homeostasis, inflammation, and impaired β-cell function

Cellular cholesterol homeostasis is important for normal β-cell function. Disruption of cholesterol transport by decreased function of the ATP-binding cassette (ABC) transporter ABCA1 results in impaired insulin secretion. Mice lacking β-cell ABCA1 have increased islet expression of ABCG1, another cholesterol transporter implicated in β-cell function. To determine whether ABCA1 and ABCG1 have complementary roles in β-cells, mice lacking ABCG1 and β-cell ABCA1 were generated and glucose tolerance, islet sterol levels, and β-cell function were assessed. Lack of both ABCG1 and β-cell ABCA1 resulted in increased fasting glucose levels and a greater impairment in glucose tolerance compared with either ABCG1 deletion or loss of ABCA1 in β-cells alone. In addition, glucose-stimulated insulin secretion was decreased and sterol accumulation increased in islets lacking both transporters compared with those isolated from knockout mice with each gene alone. Combined deficiency of ABCA1 and ABCG1 also resulted in significant islet inflammation as indicated by increased expression of interleukin-1β and macrophage infiltration. Thus, lack of both ABCA1 and ABCG1 induces greater defects in β-cell function than deficiency of either transporter individually. These data suggest that ABCA1 and ABCG1 each make complimentary and important contributions to β-cell function by maintaining islet cholesterol homeostasis in vivo.     

High glucose increases mesangial lipid accumulation via impaired cholesterol transporters

Diabetes, whether it occurs before or after transplantation, plays an important role to decrease graft function and survival. In addition renal lipid accumulation has been suggested to play a role in the development and progression of chronic renal allograft rejection. Intracellular lipid accumulation is governed by a balance between the influx and efflux of lipid. Cholesterol transporters, such as scavenger receptor (SR)-A1, CD36, and ATP binding cassette (ABC) A1 and G1 (ABCG1), coordinate to regulate cellular lipid status. Therefore, in the present study, we examined whether high glucose caused lipid accumulation in mesangial cells as a result of altered cholesterol transporters. Mouse mesangial cells were stimulated with 30 mmol/L D-glucose (high glucose); 100 μmol/L oleic acid (OA) used as a positive control. Cellular lipid accumulation was measured by Oil Red O staining. Protein and mRNA expression of cholesterol influx (SR-A1 and CD36) and efflux (ABCA1 and ABCG1) transporters were evaluated using Western blot analysis and real-time quantitative polymerase chain reaction, respectively. High glucose was shown to significantly increase lipid accumulation in mesangial cells at 24 hours as was observed for OA. SR-A1 and CD36 mRNA expression levels were 1.5-fold and 3.5-fold higher, respectively, in high glucose-stimulated than control mesangial cell, whereas ABCG1 mRNA expression decreased to 60% of controls; however, there was no decrease in ABCA1 mRNA. Altered protein expression of each transporter in mesangial cells cultured under conditions of high glucose concentrations was consistent with mRNA expression. Osmotic control using mannitol did not significantly affect any of the measured parameters in the present study. These results demonstrated that high glucose, in itself, can induce mesangial lipid accumulation; this effect may be associated with an impaired balance between the influx and efflux of cholesterol.     

Role of ABCA1 in angiotensinⅡ-induced cholesterol accumulation in podocytes

Objective To investigate the effects of angiotensinⅡ(AngⅡ) on the expression of ATP-binding cassette transporter A1(ABCA1) in AngⅡ-infused rat model and cultured human podocytes, and to explore the role of ABCA1 in AngⅡ-induced cholesterol accumulation of podocytes. Methods Twelve Wistar rats were randomly subjected to normal saline infusion, or AngⅡ infusion at 400 ng?kg-1?min-1 (via subcutaneous osmotic minipumps) for 8 weeks. The expression of glomerular ABCA1 was analyzed by Western blotting and real-time fluorescent quantitative PCR. In vitro, conditionally immortalized human podocytes were divided into normal group, AngⅡ group, AngⅡ+scrambled siRNA group, AngⅡ+ABCA1 siRNA group. The expression of podocyte ABCA1 was assessed by immunofluorescence, Western blotting and real-time fluorescent quantitative PCR. Oil Red O staining was used to observe the lipid droplets in podocytes and cholesterol efflux assay kit was used to measure the cholesterol efflux rate of podocytes. Fluorescein isothiocyanate (FITC)-conjugated phalloidin was used to observe the podocyte cytoskeleton. Results In vivo, compared with normal group, the protein and mRNA expression of glomerular ABCA1 in AngⅡ-infused rats were decreased (P＜0.05). In vitro, ABCA1 was distributed in the cytomembrane of podocytes, and compared with normal group, AngⅡtreatment down-regulated the expression of ABCA1 (P＜0.05). Increased lipid droplets, decreased cholesterol efflux and cytoskeletal rearrangement were observed in AngⅡ-treated podocytes. When compared to AngⅡ group, podocytes stimulated by AngⅡand then transfected with ABCA1 siRNA had lower expression level of ABCA1 mRNA and protein (all P＜0.05). More lipid droplets and lower cholesterol efflux rate could be observed in AngⅡ+ABCA1 siRNA group (P＜0.05). Conclusion The reduced expression of ABCA1 may be involved in AngⅡ-induced cholesterol accumulation in podocytes.     

The small GTPase Rho mediates articular chondrocyte phenotype and morphology in response to interleukin‐1α and insulin‐like growth factor‐I

Small GTPases regulate the cytoskeleton and numerous other cellular functions. In this study, the role of Rho GTPase was examined in articular chondrocytes. Chondrocytes grown in monolayer were treated with interleukin‐1α (IL‐1α), insulin‐like growth factor‐I (IGF‐I), C3 Transferase, Y27632, or transfected with Rho wild type or two constitutively active mutants of Rho (Q63L and G14V). Quantitative PCR was used to determine changes in matrix metalloproteinase‐13 (MMP‐13), collagen types IIB (COL2A1) and type I (COL1A1), aggrecan (AGG), and SOX‐9 gene expression. Affinity assays were performed to measure endogenous GTP‐bound Rho, and confocal microscopy was used to assess changes in organization of the actin cytoskeleton. IL‐1α and RhoG14V increased cytoplasmic actin stress fiber formation, which was blocked by C3 Transferase, and Y27632. IL‐1α treatment also increased Rho activity. Conversely, IGF‐I lead to formation of a cortical rim of actin and decreased Rho activity. Inhibition of Rho signaling with C3 Transferase significantly decreased Rho activity and returned IL‐1α‐induced Rho activity to a level not different from control. C3 Transferase treatment also increased mRNA expression of AGG, COL2A1, and SOX‐9, and decreased expression of MMP‐13. Expression of RhoQ63L or RhoG14V resulted in increased MMP‐13 expression; however, inhibition of Rho with Y27632 was unable to inhibit IL‐1α‐induced MMP‐13 expression. Together, these results indicate a role for increased Rho activity in mediation of chondrocyte catabolic signaling pathways. © 2008 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 27:58–64, 2009     

Temporal growth factor release from platelet‐rich plasma,trehalose lyophilized platelets,and bone marrow aspirate and their effect on tendon and ligament gene expression

Platelet‐rich plasma (PRP) has generated substantial interest for tendon and ligament regeneration because of the high concentrations of growth factors in platelet α‐granules. This study compared the temporal release of growth factors from bone marrow aspirate (BMA), PRP, and lyophilized platelet product (PP), and measured their effects on tendon and ligament gene expression. Blood and BMA were collected and processed to yield PRP and plasma. Flexor digitorum superficialis tendon (FDS) and suspensory ligament (SL) explants were cultured in 10% plasma in DMEM (control), BMA, PRP, or PP. TGF‐β1 and PDGF‐BB concentrations were determined at 0, 24, and 96 h of culture using ELISA. Quantitative RT‐PCR for collagen types I and III (COL1A1, COL3A1), cartilage oligomeric matrix protein (COMP), decorin, and matrix metalloproteinases‐3 and 13 (MMP‐3, MMP‐13) was performed. TGF‐β1 and PDGF‐BB concentrations were highest in PRP and PP. Growth factor quantity was unchanged in BMA, increased in PRP, and decreased in PP over 4 days. TGF‐β1 and platelet concentrations were positively correlated. Lyophilized PP and PRP resulted in increased COL1A1:COL3A1 ratio, increased COMP, and decreased MMP‐13 expression. BMA resulted in decreased COMP and increased MMP‐3 and MMP‐13 gene expression. Platelet concentration was positively correlated with COL1A1, ratio of COL1A1:COL3A1, and COMP, and negatively correlated with COL3A1, MMP‐13, and MMP‐3. White blood cell concentration was positively correlated with COL3A1, MMP3, and MMP13, and negatively correlated with a ratio of COL1A1:COL3A1, COMP, and decorin. These findings support further in vivo investigation of PRP and PP for treatment of tendonitis and desmitis. © 2009 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 27: 1033–1042, 2009