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1.
J Cardiovasc Pharmacol ; 67(2): 121-8, 2016 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-26371949

RESUMO

OBJECTIVE: We aimed to investigate the expression characteristics of transient receptor potential canonical 7 (TRPC7) in normal and hypertrophic cardiac myocytes. METHODS: The 2-kidney 1-clip (2K1C) method was used to induce renovascular hypertension. Losartan, the potent inhibitor of angiotensin II (Ang II) receptor, was applied to the drinking water of 2K1C rats to inhibit Ang II-mediated responses. TRPC7 expression was examined by immunohisto/cytochemistry and Western blot analyses in normal and hypertrophic hearts. The expression level of protein kinase C (PKC), a negative regulator of TRPC7 channel in in vitro study, was also evaluated. RESULTS: In normal rat ventricles, strong TRPC7 immunoreactivity was distributed in the surface sarcolemma of cardiomyocytes, and a moderate but striated TRPC7 immunoreactivity was also detected in the subcellular regions. The 2K1C operation caused significant hypertension and cardiac hypertrophy as demonstrated by respective biophysical or biochemical assays. At this stage, expression of TRPC7 was significantly downregulated at both tissue and cell levels, whereas that of PKC was upregulated. Further analysis revealed a negative correlation between TRPC7 and PKC expression patterns. Oral application of losartan ameliorated the extent of experimentally induced hypertension and cardiac hypertrophy. Simultaneously, it effectively reversed the downregulation of TRPC7 and mildly antagonized the upregulation of PKC. CONCLUSIONS: Taken together, these results for the first time show that TRPC7 localizes in the surface and tubular sarcolemma of cardiomyocytes in normal adult rats and its expression significantly decreases in hypertrophied cardiomyocytes from renovascular hypertensive rats. TRPC7 may thus play a significant role in normal physiological settings in the heart.

2.
Onco Targets Ther ; 5: 403-7, 2012.
Artigo em Inglês | MEDLINE | ID: mdl-23226027

RESUMO

BACKGROUND: The PER1 circadian-clock gene plays an important role in the regulation of many normal physiological rhythms in vivo. It has been revealed recently that abnormal expression of PER1 correlates closely with the occurrence and development of many cancers. However, the expression and significance of PER1 in oral squamous cell carcinoma (OSCC) remains unknown. The purpose of the present study was to investigate the direct links between aberrant PER1 expression and clinicopathological features of OSCC. METHODS: PER1 expression in cancerous and adjacent noncancerous tissues from 41 patients with OSCC was detected by immunohistochemical staining and real-time reverse transcriptase polymerase chain reaction, and correlations were sought with clinicopathological features in patients. RESULTS: Expression of PER1 mRNA and protein in OSCC was significantly reduced compared with that in adjacent noncancerous tissue (P < 0.05). Expression of PER1 protein in oral phase III-IV SCC specimens was significantly lower than that in phase I-II specimens (P < 0.05), and stage T(1)-T(2) patients expressed significantly higher levels of PER1 protein than T(3)-T(4) patients (P < 0.05). Expression of PER1 in patients without lymph node metastasis was significantly higher than that in those with lymph node metastasis (P < 0.05). PER1 protein expression showed no significant correlation with patient gender and age, or with degree of tumor cell differentiation (P > 0.05). CONCLUSION: Changes in PER1 expression may play an important role in the development, invasion, and metastasis of OSCC, and may also provide novel ideas and methods for investigation of the occurrence, development, and targeted treatment OSCC.

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