Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated whether expression of non-selective cation channels of the transient receptor potential canonical (TRPC) channel family are associated with proinflammatory cytokines in monocytes. Using quantitative RT-PCR we studied the expression of TRPC3, interleukin-1beta (IL-1beta), and tumor necrosis factor-alpha (TNF-alpha) in monocytes from 15 patients with essential hypertension and 16 age- and sex-matched normotensive control subjects. We observed an approximately 8-fold increase of TRPC3 transcripts in monocytes from patients with essential hypertension compared to normotensive control subjects (p<0.05). We found an approximately 3-fold increase of IL-1beta, and an approximately 9-fold increase of TNF-alpha in patients with essential hypertension compared to normotensive control subjects (each p<0.05). We observed a significant correlation between TRPC3 transcripts with systolic blood pressure, expression of IL-1beta, and TNF-alpha. Using quantitative RT-PCR we observed an association of TRPC3 transcripts and proinflammatory cytokines in monocytes.
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PMID:Association of transient receptor potential canonical type 3 (TRPC3) channel transcripts with proinflammatory cytokines. 1817 30

Transient Receptor Potential Canonical (TRPC) proteins are non-selective cation channels ubiquitously expressed throughout the cardiovascular system, where they participate as Ca2+/Na+-permeable channels and/or signaling platforms in various physiological and pathophysiological mechanisms. TRPCs have been implicated in essential hypertension, cardiac hypertrophy and endothelial dysfunction. Despite these pathologies being related, directly or indirectly to development of atherosclerotic lesions, the potential role of TRPCs in the pathogenesis of atherosclerosis remains unexplored. Recent studies from our laboratory showing an obligatory requirement of TRPC3 in the inflammatory signaling linked to monocycle recruitment to coronary endothelium, suggest for the first time potential pathophysiological relevance of a member of the TRPC group in atherogenesis. This brings about the question whether we can envision TRPCs as potential targets for diagnosis, prognosis and/or treatment of atherosclerosis. Here we revisit some of the existing knowledge on TRPCs and cardiovascular pathology and discuss it within the context of cellular/molecular processes related to atherogenesis. Potential limitations and advantages of TRPCs as prospectives targets in atherosclerosis are discussed and confronted against.
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PMID:TRPC channels as prospective targets in atherosclerosis: terra incognita. 2220 50