Search Results
You are looking at 1 - 7 of 7 items for
- Author: Haiyan Zhang x
- Refine by access: All content x
Search for other papers by Meijia Zhang in
Google Scholar
PubMed
Search for other papers by Haiyan Hong in
Google Scholar
PubMed
Search for other papers by Bo Zhou in
Google Scholar
PubMed
Search for other papers by Shiying Jin in
Google Scholar
PubMed
Search for other papers by Chao Wang in
Google Scholar
PubMed
Search for other papers by Maoyong Fu in
Google Scholar
PubMed
Search for other papers by Songbo Wang in
Google Scholar
PubMed
Search for other papers by Guoliang Xia in
Google Scholar
PubMed
Locally synthesized atrial natriuretic peptide (ANP) and its receptors have been found in reproductive tissues of various mammals, and play an important role in the acrosome reaction of human sperm. The objective of the present study was to examine the expression of ANP and its receptors in pig spermatozoa and oviduct, and the effect of ANP on pig spermatozoa function. The expression of ANP and its receptors was analyzed by RT-PCR. Only natriuretic peptide receptors-A (NPRA) mRNA was detected in fresh sperm. While the levels of natriuretic peptide receptors-C (NPRC) mRNA were low with no obvious change among different oviductal phases, the levels of ANP mRNA were high in oviduct(OT)1 , OT3 and OT5, but were very low in OT2. On the other hand, the levels of NPRA mRNA were low in OT1 and OT2, increased in OT3 and reached a maximum in OT4 and OT5. Western blot analysis revealed that the level of ANP was high in OT1, decreased in OT2 and OT3, and arrived at the nadir in OT4 and OT5. The effect of ANP on spermatozoa function was studied by the acrosome reaction and IVF. Incubation with ANP for 1 h significantly induced acrosome reaction of preincubated spermatozoa, and maximal response of acrosome reaction (34.1 ± 2.3%) was achieved at 1 nM ANP treatment. Both C-ANP-(4–23), a selective ligand of NPRC, and caffeine had no effect on the acrosome reaction. The stimulatory effect of ANP on acrosome reaction could be mimicked by the permeable cGMP analog, 8-Br-cGMP. ANP and caffeine had a similar effect on improving the oocytes penetration rate, polyspermy rate and the average number of sperm per penetrated oocyte. Also, ANP treatment had a similar effect on cleavage rate, blastocyst formation rate and the number of cells per blastocyst as that of caffeine treatment. The effects of ANP on the acrosome reaction and the parameters of oocyte penetration could be blocked by cGMP-dependent protein kinase (PKG) inhibitors KT5823 and/or Rp-8-pCPT-cGMPS. These results suggest that the expression of ANP in the oviduct may be involved in the regulation of the acrosome reaction and the fertilising ability of pig spermatozoa, and the PKG pathway possibly participates in the process.
Search for other papers by Parveen Abidi in
Google Scholar
PubMed
Search for other papers by Haiyan Zhang in
Google Scholar
PubMed
Search for other papers by Syed M Zaidi in
Google Scholar
PubMed
Search for other papers by Wen-Jun Shen in
Google Scholar
PubMed
Search for other papers by Susan Leers-Sucheta in
Google Scholar
PubMed
Search for other papers by Yuan Cortez in
Google Scholar
PubMed
Search for other papers by Jiahuai Han in
Google Scholar
PubMed
Department of Veterans Affairs Palo Alto Health Care System, Division of Gastroenterology and Hepatology, Department of Immunology, Geriatric Research, Education and Clinical Center (GRECC), 3801 Miranda Avenue, Palo Alto, California 94304, USA
Search for other papers by Salman Azhar in
Google Scholar
PubMed
Previous studies from this laboratory identified excessive oxidative stress as an important mediator of age-related decline in steroid hormone production. Here, we investigated whether oxidative stress exerts its antisteroidogenic action through modulation of oxidant-sensitive mitogen-activated protein kinase (MAPK) signaling pathways. To accomplish these studies, we employed a highly responsive mouse adrenocortical cell line, Y1-BS1 cells that secrete large quantities of steroids when stimulated with lipoprotein plus hormone. Treatment of these cells with superoxide, H2O2 or 4-hydroxy-2-nonenal (HNE) significantly inhibited steroid production and increased phosphorylation and activation of p38 MAPK. None of the treatments altered the phosphorylation of either extracellular signal-regulated kinases or c-Jun N-terminal kinases (JNKs). Pretreatment of Y1-BS1 cells with MnTMPyP, a cell-permeable superoxide-dismutase/catalase mimetic reactive oxygen species (ROS scavenger), completely prevented the superoxide- and H2O2-mediated inhibition of steroid production. Likewise, antioxidant N-acetylcysteine completely blocked the HNE-induced loss of steroidogenic response. Incubation of Y1-BS1 cells with either MnTMPyP or NAC also upregulated Bt2cAMP and Bt2cAMP+hHDL3-stimulated steroid synthesis, indicating that endogenously produced ROS can inhibit steroidogenesis. Inhibition of p38 MAPK with SB203580 or SB202190 upregulated the basal steroid production and also prevented the oxidant-mediated inhibition of steroid production. mRNA measurements by qPCR indicated that Y1-BS1 adrenal cells predominantly express p38 MAPKα isoform, along with relatively low-level expression of p38 MAPKγ. By contrast, little or no expression was detected for p38 MAPKβ and p38 MAPKδ isoforms in these cells. Transfection of Y1-BS1 cells with either caMKK3 or caMMK6 construct, the upstream p38 MAPK activators, decreased steroidogenesis, whereas transfection with dnMKK3 or dnMKK6 plasmid DNA increased steroidogenesis. Similarly, transfection of cells with a dnp38 MAPKα or dnp38 MAPKβ construct also increased steroid hormone production; however, the effect was less pronounced after expression of either dnp38 MAPKγ or dnp38 MAPKδ construct. These results indicate that activated p38 MAPK mediates oxidant (excessive oxidative stress)-induced inhibition of adrenal steroidogenesis.
Search for other papers by Xiuli Men in
Google Scholar
PubMed
Search for other papers by Liang Peng in
Google Scholar
PubMed
Search for other papers by Haiyan Wang in
Google Scholar
PubMed
Search for other papers by Wenjian Zhang in
Google Scholar
PubMed
Search for other papers by Shiqing Xu in
Google Scholar
PubMed
Search for other papers by Qing Fang in
Google Scholar
PubMed
Search for other papers by Honglin Liu in
Google Scholar
PubMed
Search for other papers by Wenying Yang in
Google Scholar
PubMed
Search for other papers by Jinning Lou in
Google Scholar
PubMed
The calcium-regulated transcription coactivator, Ca2 +-responsive transactivator (CREST) was expressed in pancreatic β-cells. Moreover, CREST expression became significantly increased in pancreatic islets isolated from hyperglycemic Goto–Kakizaki rats compared with normoglycemic Wistar controls. In addition, culture of β-cells in the presence of high glucose concentrations also increased CREST expression in vitro. To further investigate the role of this transactivator in the regulation of β-cell function, we established a stable β-cell line with inducible CREST expression. Hence, CREST overexpression mimicked the glucotoxic effects on insulin secretion and cell growth in β-cells. Moreover, high glucose-induced apoptosis was aggravated by upregulation of the transactivator but inhibited when CREST expression was partially silenced by siRNA technology. Further investigation found that upregulation of Bax and downregulation of Bcl2 was indeed induced by its expression, especially under high glucose conditions. In addition, as two causing factors leading to β-cell apoptosis under diabetic conditions, endoplasmic reticulum stress and high free fatty acid, mimicked the high glucose effects on CREST upregulation and generation of apoptosis in β-cells, and these effects were specifically offset by the siRNA knockdown of CREST. These results indicated that CREST is implicated in β-cell apoptosis induced by culture in high glucose and hence that CREST may become a potential pharmacological target for the prevention and treatment of type 2 diabetes mellitus.
Graduate School of Peking Union Medical College, Institute of Clinical Medical Sciences, Department of Cell Physiology and Metabolism, Beijing 100730, People's Republic of China
Search for other papers by Bo Qian in
Google Scholar
PubMed
Search for other papers by Haiyan Wang in
Google Scholar
PubMed
Search for other papers by Xiuli Men in
Google Scholar
PubMed
Search for other papers by Wenjian Zhang in
Google Scholar
PubMed
Search for other papers by Hanqing Cai in
Google Scholar
PubMed
Search for other papers by Shiqing Xu in
Google Scholar
PubMed
Search for other papers by Yaping Xu in
Google Scholar
PubMed
Search for other papers by Liya Ye in
Google Scholar
PubMed
Search for other papers by Claes B Wollheim in
Google Scholar
PubMed
Search for other papers by Jinning Lou in
Google Scholar
PubMed
We found that TRIB3, an endogenous inhibitor of Akt (PKB), is expressed in pancreatic β-cells. The TRIB3 expression is significantly increased in islets isolated from hyperglycemic Goto–Kakizaki rats compared with normal glycemic controls. In vitro high glucose treatment also resulted in increased TRIB3 expression in rat INS1 cells. To investigate the role of TRIB3 in the regulation of β-cell function, we established an INS1 stable cell line allowing inducible expression of TRIB3. We demonstrated that overexpression of TRIB3 mimicked the glucotoxic effects on insulin secretion and cell growth in INS1 cells. Moreover, induction of TRIB3 also synergistically enhanced high-glucose-elicited apoptosis in INS1 cells, whereas siRNA knock-down of TRIB3 showed the opposite effects. We also confirmed that the ΔΨm of mitochondria was decreased, caspase-3 activity was up-regulated and reactive oxygen species content was increased in TRIB3 overexpressing β cells in high glucose condition. Most interestingly, the oestrogen receptor (ER) stress inducer, thapsigargin, mimicked the high glucose effects on up-regulation of TRIB3 and generation of apoptosis in cultured INS1 cells. These effects were specifically prevented by siRNA knock down of TRIB3. We therefore conclude that TRIB3 is implicated in glucotoxicity- and ER stress-induced β-cell failure. TRIB3 could be a potential pharmacological target for prevention and treatment of type 2 diabetes.
Search for other papers by Bo Qian in
Google Scholar
PubMed
Search for other papers by Haiyan Wang in
Google Scholar
PubMed
Search for other papers by Xiuli Men in
Google Scholar
PubMed
Search for other papers by Wenjian Zhang in
Google Scholar
PubMed
Search for other papers by Hanqing Cai in
Google Scholar
PubMed
Search for other papers by Shiqing Xu in
Google Scholar
PubMed
Search for other papers by Yaping Xu in
Google Scholar
PubMed
Search for other papers by Liya Ye in
Google Scholar
PubMed
Search for other papers by Claes B Wollheim in
Google Scholar
PubMed
Search for other papers by Jinning Lou in
Google Scholar
PubMed
Search for other papers by Bo Qian in
Google Scholar
PubMed
Search for other papers by Haiyan Wang in
Google Scholar
PubMed
Search for other papers by Xiuli Men in
Google Scholar
PubMed
Search for other papers by Wenjian Zhang in
Google Scholar
PubMed
Search for other papers by Hanqing Cai in
Google Scholar
PubMed
Search for other papers by Shiqing Xu in
Google Scholar
PubMed
Search for other papers by Yaping Xu in
Google Scholar
PubMed
Search for other papers by Liya Ye in
Google Scholar
PubMed
Search for other papers by Claes B Wollheim in
Google Scholar
PubMed
Search for other papers by Jinning Lou in
Google Scholar
PubMed
Search for other papers by Qiongge Zhang in
Google Scholar
PubMed
Search for other papers by Chaoqun Wang in
Google Scholar
PubMed
Search for other papers by Yehua Tang in
Google Scholar
PubMed
Search for other papers by Qiangqiang Zhu in
Google Scholar
PubMed
Search for other papers by Yongcheng Li in
Google Scholar
PubMed
Search for other papers by Haiyan Chen in
Google Scholar
PubMed
Search for other papers by Yi Bao in
Google Scholar
PubMed
Search for other papers by Song Xue in
Google Scholar
PubMed
Search for other papers by Liangliang Sun in
Google Scholar
PubMed
Search for other papers by Wei Tang in
Google Scholar
PubMed
Search for other papers by Xiangfang Chen in
Google Scholar
PubMed
Search for other papers by Yongquan Shi in
Google Scholar
PubMed
Search for other papers by Lefeng Qu in
Google Scholar
PubMed
Search for other papers by Bin Lu in
Google Scholar
PubMed
Search for other papers by Jiaoyang Zheng in
Google Scholar
PubMed
Hyperglycemia plays a major role in the development of diabetic macrovascular complications, including atherosclerosis and restenosis, which are responsible for the most of disability and mortality in diabetic patients. Osteopontin (OPN) is an important factor involved in atherogenesis, and hyperglycemia enhances the transcriptional activity of FoxO1 which is closely association with insulin resistance and diabetes. Here, we showed that plasma OPN levels were significantly elevated in type 2 diabetic patients and positively correlated with glycated albumin (GA). The more atherosclerotic lesions were observed in the aorta of diabetic ApoE−/− mice analyzed by Sudan IV staining. High glucose increased both the mRNA and protein expression levels of OPN and inhibited the phosphorylation of FoxO1 in RAW 264.7 cells. Overexpression of WT or constitutively active mutant FoxO1 promoted the expression levels of OPN, while the dominant-negative mutant FoxO1 decreased slightly the expression of OPN. Conversely, knockdown of FoxO1 reduced the expression of OPN. Luciferase reporter assay revealed that high glucose and overexpression of FoxO1 enhanced the activities of the OPN promoter region nt −1918 ~ −713. Furthermore, the interactions between FoxO1 and the OPN promoter were confirmed by electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation assay (ChIP). Our results suggest that high glucose upregulates OPN expression via FoxO1 activation, which would play a critical role in the development of diabetic atherogenesis.
