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Articles by Qiang Ding
Total Records ( 2 ) for Qiang Ding
  Jing Wang , Liping Zhang , Jianping Wu , Jianlei Jia and Qiang Ding
  Association between lambing performance (single lamb and twins) and reproductive hormones has been explored. Twenty four ewes divided into 4 groups of each 6 individuals were sampled according to the number of lambs in two breeds (Mongolian ewes and Poll Dorset ewes) blood samples from each individual ewe were collected at the three periods: estrus (day 0) estrus (day 11) and post-partum anoestrus. All the seven hormones concentration of the Poll Dorset ewes was higher than that of the Mongolian ewes in the three periods. And the hormones secretion shown different patterns in two breeds. Five hormones concentrations of ewes with twins were higher than that of ewes with single lamb, the reverse situation found in MT and T concentration even a few of them were statistically significant (p<0.05) at the three periods. Finally, the highly positive and negative significant correlations between hormones were detected, this relationship also shown the differences in two breeds.
  Qiang Ding , Candece L. Gladson , Hongju Wu , Haurko Hayasaka and Mitchell A. Olman
  Transforming growth factor (TGF)-β1 induces fibroblast transdifferentiation to myofibroblasts, a process that requires the involvement of integrin-mediated signaling and focal adhesion kinase (FAK). FAK-related non-kinase (FRNK) is known for its role in inhibiting integrin-mediated cell migration; however, its role in myofibroblast differentiation has not been defined. Here, we report that FRNK abrogates TGF-β1-induced myofibroblast differentiation in vitro and in vivo. TGF-β1 can induce α-smooth muscle actin (α-SMA) expression in the presence or absence of FAK; however, TGF-β1-induced α-SMA expression is reduced (~73%) in FAK-deficient fibroblasts. Although both ERK and p38 MAPK activation is required for maximal TGF-β1-induced α-SMA expression, ERK is the major signaling intermediate in cells that express FAK. In contrast, p38 MAPK is the dominant mediator of TGF-β1-induced α-SMA expression in FAK-deficient cells. FRNK overexpression blocks TGF-β1-induced ERK or p38 MAPK activation in the presence, and surprisingly, in the absence of FAK. The loss of FRNK was tested in vivo during experimentally induced pulmonary fibrosis in mice. FRNK knock-out mice have a greater increase in α-SMA-expressing cells in response to a pulmonary fibrotic stimulus in vivo, as compared with congenic wild type mice. This is the first time that FRNK loss has been shown to modify the pathobiology in any animal disease model. Together, the data demonstrate that FRNK negatively regulates myofibroblast differentiation in vitro and in vivo. These data further suggest that modulation FRNK expression may be a novel avenue for therapeutic intervention in tissue fibrosis.
 
 
 
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