In:
Annals of the New York Academy of Sciences, Wiley, Vol. 976, No. 1 ( 2002-11), p. 237-247
Abstract:
A bstract : The Na + /Ca 2+ exchanger (NCX1) is regulated at the transcriptional level in cardiac hypertrophy, ischemia, and failure. Following pressure overload, activation of MAPKs coincides with the kinetics of NCX1 gene upregulation in adult cardiocytes. Using adenoviral gene delivery, we begin to identify the molecular pathways responsible for upregulation of the exchanger gene. Inhibition of ERK with the MEK inhibitor UO126, the ERK protein phosphatase MKP‐3, inhibited ERK activation, but only inhibited α‐adrenergic‐induced NCX1 upregulation by 30%. Overexpression of DN‐JNK lowered basal NCX1 expression. Overexpression of activated MKK‐3 was sufficient for α‐adrenergic‐stimulated upregulation of the reporter gene. Together, this data indicates that (1) JNK mediates basal cardiac expression of the NCX1 gene, (2) ERK and p38 play a role in α‐adrenergic‐stimulated NCX1 upregulation, and (3) p38 activation alone is sufficient for NCX1 upregulation.
Type of Medium:
Online Resource
ISSN:
0077-8923
,
1749-6632
DOI:
10.1111/nyas.2002.976.issue-1
DOI:
10.1111/j.1749-6632.2002.tb04746.x
Language:
English
Publisher:
Wiley
Publication Date:
2002
detail.hit.zdb_id:
2834079-6
detail.hit.zdb_id:
211003-9
detail.hit.zdb_id:
2071584-5
SSG:
11
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