In current study, the expressions of protein kinase C (PKC)-alpha, beta I and beta II as well as their correlation to the expression of transforming growth factor-beta I (TGF-beta I) and vascular endothelial growth factor (VEGF) were investigated in glomeruli of normal renal tissues taken from human kidney tumors and kidney tissues from patients with diabetic nephropathy (DN). The accumulation of glomerular extracellular matrix (ECM) was determined by PAS staining, the expressions of PKC-a, PKC-beta I, PKC-beta II, TGF-beta I and VEGF were measured by semi-quantitative immunohistochemistry. Our results showed that in glomeruli of normal renal tissues, PKC-alpha and beta II had a strong expression whereas the expression of PKC-beta I was weak; in glomeruli of DN patients, the expressions of PKC-alpha, PKC-beta I, VEGF and TGF-beta I and the accumulation of ECM increased significantly, but the expression of PKC-beta II decreased markedly. Meanwhile, the expressions of PKC-alpha and beta I had a positive correlation to the expressions of VEGF and TGF-beta I respectively, whereas PKC-beta II showed no correlation to VEGF and TGF-beta I. It is concluded that the expressions of PKC-alpha, beta I and beta II in glomeruli of normal subjects and DN patients are different. PKC-alpha seems to play a critical role in human DN by up-regulating VEGF expression, whereas PKC-beta I is relatively important for the up-regulation of TGF-beta I and the accumulation of ECM under diabetic conditions.
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http://dx.doi.org/10.1007/s11596-006-0605-5 | DOI Listing |
J Am Heart Assoc
February 2024
Division of Cardiothoracic Surgery, Rhode Island Hospital Alpert Medical School of Brown University Providence RI.
Background: Small conductance calcium-activated potassium (SK) channels are largely responsible for endothelium-dependent coronary arteriolar relaxation. Endothelial SK channels are downregulated by the reduced form of nicotinamide adenine dinucleotide (NADH), which is increased in the setting of diabetes, yet the mechanisms of these changes are unclear. PKC (protein kinase C) is an important mediator of diabetes-induced coronary endothelial dysfunction.
View Article and Find Full Text PDFInt J Mol Sci
July 2023
Key Laboratory of Prevention and Control Agents for Animal Bacteriosis (Ministry of Agriculture and Rural Affairs), Hubei Provincial Key Laboratory of Animal Pathogenic Microbiology, Institute of Animal Husbandry and Veterinary, Hubei Academy of Agricultural Sciences, Wuhan 430064, China.
(APP) is the causative pathogen of porcine pleuropneumonia, a highly contagious respiratory disease in the pig industry. The increasingly severe antimicrobial resistance in APP urgently requires novel antibacterial alternatives for the treatment of APP infection. In this study, we investigated the effect of tea polyphenols (TP) against APP.
View Article and Find Full Text PDFReprod Biol
June 2023
Endocrinology Division, CSIR-Central Drug Research Institute, Lucknow, India. Electronic address:
We investigated the role of protein kinase c (PKC) -α and -β during the ovarian follicular dynamics using estrous cycle, gonadotropin-induced ovulation, and antral follicle culture, 4-vinylcyclohexene diepoxide (VCD)-induced premature ovarian failure (POF) in the SD rat models. We found the higher activity of PKC during the proestrus stage along with expression of PKC-α during the estrus and metestrus stages of the estrous cycle while PKC-β expression was increased during the diestrus, proestrus, and estrus stages. In response to pregnant mare gonadotropin (PMSG)-induced follicular recruitment and ovulation, the phosphorylated (Thr-642) PKC-β was increased.
View Article and Find Full Text PDFOxid Med Cell Longev
February 2023
Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai 200040, China.
Background: Studies that looked at asthma airway remodeling pathogenesis and prevention have led to the discovery of the rat sarcoma viral oncogene (RAS) signaling pathway as a key mechanism that controls airway smooth muscle cell (ASMC) proliferation. Baicalin has great anti-inflammatory, proliferation-inhibited, and respiratory disease-relieving properties. However, the inhibitory effects and mechanisms of baicalin on ASMC-mediated airway remodeling in mice are still poorly understood.
View Article and Find Full Text PDFAm J Physiol Cell Physiol
August 2023
Montreal Heart Institute, Université de Montréal, Montreal, Quebec, Canada.
The present study tested the hypothesis that protein kinase C-α (PKC-α) recruitment in the presence of the p38α/β MAPK inhibitor SB203580 facilitated the appearance and cell cycle re-entry of nestin-neonatal rat ventricular cardiomyocytes (NNVMs) and induced a transcript profile delineating a proliferative phenotype. Phorbol 12,13-dibutyrate (PDBu) treatment did not induce de novo nestin expression or increase the cell cycle re-entry of 1-day-old NNVMs but significantly increased runt-related transcription factor 1 (Runx1) and p16 cell cycle inhibitor (CDKN2a) mRNA levels and downregulated epithelial cell transforming 2 (ECT2) mRNA expression. SB203580 administration to PDBu-treated NNVMs induced de novo nestin expression, preferentially increased the density (normalized to 500 NNVMs) of nestin-NNVMs that incorporated 5-bromo-2'-deoxyuridine (PDBu, 1.
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