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Cell mechanics studied by a reconstituted model tissue

BIOPHYSICAL JOURNAL 2000年第5期79卷 2353-2368页

作者： Wakatsuki, T Kolodney, MS Zahalak, GI Elson, EL Washington Univ Sch Med Dept Biochem & Mol Biophys St Louis MO 63110 USA Univ Calif Los Angeles Sch Med MacDonald Res Lab 1519 Dept MedDiv Dermatol Los Angeles CA 90095 USA Washington Univ Sch Engn Dept Biomed Engn St Louis MO 63130 USA Washington Univ Sch Engn Dept Mech Engn St Louis MO 63130 USA

Tissue models reconstituted from cells and extracellular matrix (ECM) simulate natural tissues. Cytoskeletal and matrix proteins govern the force exerted by a tissue and its stiffness. Cells regulate cytoskeletal structure and remodel ECM to produce mechanical changes during tissue development and wound healing. Characterization and control of mechanical properties of reconstituted tissues are essential for tissue engineering applications. We have quantitatively characterized mechanical properties of connective tissue models, fibroblast-populated matrices (FPMs), via uniaxial stretch measurements. FPMs resemble natural tissues in their exponential dependence of stress on strain and linear dependence of stiffness on force at a given strain. Activating cellular contractile forces by calf serum and disrupting F-actin by cytochalasin D yield "active" and "passive" components, which respectively emphasize cellular and matrix mechanical contributions. The strain-dependent stress and elastic modulus of the active component were independent of cell density above a threshold density. The same quantities for the passive component increased with cell number due to compression and reorganization of the matrix by the cells.

关键词：生物力学细胞计数细胞培养的结缔组织细胞/生理学细胞骨架/生理学弹性细胞外基质/生理学成纤维细胞/生理学模型生物学动物鸡胚

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Gi-mediated activation of mitogen-activated protein kinase (MAPK) pathway by receptor mimetic basic secretagogues of connective tissue-type mast cells: Bifurcation of arachidonic acid-induced release upstream of MAPK

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 1999年第3期289卷 1654-1661页

作者： Shefler, I Seger, R Sagi-Eisenberg, R Tel Aviv Univ Sackler Fac Med Dept Cell Biol & Histol IL-69978 Tel Aviv Israel Weizmann Inst Sci Dept Regulat Biol IL-76100 Rehovot Israel

The family of basic secretagogues of connective tissue mast cells act as receptor mimetic agents, which trigger exocytosis by directly activating G proteins. We now demonstrate that pertussis toxin (Ptx)-sensitive Gi proteins, activated by compound 48/80 (c48/80), a potent member of this family, also activate the p42/p44 MAP kinases (MAPKs). This activation was potentiated by the protein tyrosine phosphatase inhibitor vanadate, whereas the tyrphostin AG-18, a competitive inhibitor of protein tyrosine kinases (PTKs);the protein kinase C inhibitors K252a and GF109203X;the phosphatidylinositol-3-kinase (PI-3K) inhibitors wortmannin and LY294002;and EGTA have abolished this activation. These results suggest that c48/80 activated the p42/p44 MAPKs via a mechanism that involves PTKs, protein kinase C, phosphatidylinositol-3-kinase and Ca2+ as mediators. Protein tyrosine phosphorylation and activation of the p42/p44 MAPKs were closely correlated with stimulation of arachidonic acid (AA) release by c48/80 but not with histamine secretion. However, whereas PD98059, the inhibitor of the MAPK kinase has abrogated MAPK activation, this inhibitor failed to effect release of AA. We therefore conclude that by activating Ptx-sensitive Gi protein(s), the basic secretagogues of mast cells stimulate multiple signaling pathways, which diverge to regulate the production and release of the different inflammatory mediators. Whereas the signaling pathway responsible for triggering histamine release is PTK independent, the pathway responsible for the stimulation of AA release bifurcates downstream to PTKs but upstream to the activation of MAPKs.

关键词：雄二烯类/药理学花生四烯酸类/代谢卡唑类/药理学色酮类/药理学结缔组织细胞/细胞学结缔组织细胞/生理学依他酸/药理学酶激活酶抑制剂/药理学 GTP结合蛋白质α亚单位 Gi-Go/代谢组胺释放肌醇磷酸类/代谢动力学肥大细胞/细胞学肥大细胞/药物作用肥大细胞/生理学丝裂原活化蛋白激酶1/代谢丝裂原活化蛋白激酶3 丝裂原激活蛋白激酶类吗啉类/药理学百白咳毒素磷酸酪氨酸/代谢大鼠 Wistar 信号传导酪氨酸磷酸化抑制剂/药理学钒酸盐类/药理学毒力因子鲍特菌属/药理学 p-甲氧基-N-苯丙胺/药理学动物大鼠

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The DNA binding protein BTEB mediates acetaldehyde-induced, Jun N-terminal kinase-dependent αI(I) collagen gene expression in rat hepatic stellate cells

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MOLECULAR AND CELLULAR BIOLOGY 2000年第8期20卷 2818-2826页

作者： Chen, AP Davis, BH Univ Chicago Med Ctr Dept Med Gastroenterol Sect Chicago IL 60637 USA

Alcohol-induced cirrhosis results partially from the excessive production of collagen matrix proteins, which, predominantly alpha I(I) collagen, are produced and secreted by activated hepatic stellate cells (NSC). The accumulation of alpha I(I) collagen in HSC during cirrhosis is largely due to an increase in alpha I(I) collagen gene expression. Acetaldehyde, the major active metabolite of alcohol, is known to stimulate alpha I(I) collagen production in HSC. However, the mechanisms responsible for it remain unknown. The aim of this study was to elucidate the mechanisms by which alpha I(I) collagen gene expression is induced by acetaldehyde in rat HSC. In the present study, the acetaldehyde response element was located in a distal GC box, previously described as the UV response element, in the promoter of the alpha I(I) collagen gene (-1484 to - 1476). The CC box was predominantly bound by the DNA binding transcription factor BTEB (basic transcription element binding protein), expression of which was acetaldehyde and UV inducible. Blocking BTEB protein expression significantly reduced the steady-state levels of the acetaldehyde-induced alpha I(I) collagen mRNA, suggesting that BTEB is required for this gene expression. Further studies found that acetaldehyde activated Jun N-terminal kinase (JNK) 1 and 2 and activator protein 1 (AP-1) transactivating activity. Inhibition of JNK activation resulted in the reduction of the acetaldehyde-induced BTEB protein abundance and alpha I(I) collagen mRNA levels, indicating that the expression of both genes is JNK dependent in HSC, Taken together, these studies demonstrate that BTEB mediates acetaldehyde-induced, JNK-dependent alpha I(I) collagen gene expression in HSC.

关键词：乙醛/药理学胶原/生物合成胶原/遗传学结缔组织细胞/生理学 DNA结合蛋白质类/遗传学 DNA结合蛋白质类/代谢基因表达调控/药物作用 JNK丝裂原活化蛋白激酶类 Kruppel样转录因子类肝丝裂原激活蛋白激酶类/遗传学丝裂原激活蛋白激酶类/代谢大鼠 Sprague-Dawley 信号传导/药物作用转录因子/遗传学转录因子/代谢锌指动物男(雄)性大鼠

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The role of the fibroblast in collagen turnover in the functioning periodontal ligament of the mouse

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Archives of Oral Biology 1974年第4期19卷 339-340,IN9页

作者： Cate, A.R.Ten Deporter, D.A. Faculty of Dentistry Toronto M5G 1G6 124 Edward St Canada

Examination of fibroblasts within the periodontal ligament of functioning lower first molars with the electron microscope revealed the frequent occurrence of membrane-bound intracytoplasmic profiles containing banded collagen. Residual bodies containing banded collagen were also noted These findings are similar to those made of fibroblasts associated with remodelling connective tissue. It is therefore suggested that the cellular basis for connective tissue turnover is the same as for connective tissue remodelling, namely the fibroblast. © 1974.

关键词：胶原/代谢结缔组织细胞/代谢结缔组织细胞/生理学结缔组织细胞/超微结构成纤维细胞/生理学成纤维细胞/超微结构下颌骨显微镜检查电子磨牙牙周膜/代谢牙周膜/生理学牙周膜/超微结构动物小鼠

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