{"_buckets": {"deposit": "08954b02-74ad-4f10-98c2-5c01ffc88efc"}, "_deposit": {"created_by": 1, "id": "1140", "owners": [1], "pid": {"revision_id": 0, "type": "depid", "value": "1140"}, "status": "published"}, "_oai": {"id": "oai:ir.soken.ac.jp:00001140", "sets": ["22"]}, "author_link": ["9437", "9436", "9435"], "item_1_biblio_info_21": {"attribute_name": "書誌情報（ソート用）", "attribute_value_mlt": [{"bibliographicIssueDates": {"bibliographicIssueDate": "2003-09-30", "bibliographicIssueDateType": "Issued"}, "bibliographic_titles": [{}]}]}, "item_1_creator_2": {"attribute_name": "著者名", "attribute_type": "creator", "attribute_value_mlt": [{"creatorNames": [{"creatorName": "浦本, 裕美"}], "nameIdentifiers": [{"nameIdentifier": "9435", "nameIdentifierScheme": "WEKO"}]}]}, "item_1_creator_3": {"attribute_name": "フリガナ", "attribute_type": "creator", "attribute_value_mlt": [{"creatorNames": [{"creatorName": "ウラモト, ヒロミ"}], "nameIdentifiers": [{"nameIdentifier": "9436", "nameIdentifierScheme": "WEKO"}]}]}, "item_1_date_granted_11": {"attribute_name": "学位授与年月日", "attribute_value_mlt": [{"subitem_dategranted": "2003-09-30"}]}, "item_1_degree_grantor_5": {"attribute_name": "学位授与機関", "attribute_value_mlt": [{"subitem_degreegrantor": [{"subitem_degreegrantor_name": "総合研究大学院大学"}]}]}, "item_1_degree_name_6": {"attribute_name": "学位名", "attribute_value_mlt": [{"subitem_degreename": "博士（理学）"}]}, "item_1_description_1": {"attribute_name": "ID", "attribute_value_mlt": [{"subitem_description": "2003517", "subitem_description_type": "Other"}]}, "item_1_description_12": {"attribute_name": "要旨", "attribute_value_mlt": [{"subitem_description": "The physiological or pathophysiological function of cardiac CFTR (cCFTR) is not well known. In this study, she examined whether CFTR is expressed and functioning as a Cl\u003cSUP\u003e-\u003c/SUP\u003e channel in ischemic cardiomyocytes and whether cCFTR plays a role in protection from ischemic injury in neonatal rat ventricular cardiomyocytes in primary culture. After the cells were subjected to ischemia, time-dependent changes in CFTR expression were examined in the membrane fraction by western blot. A peak expression of mature CFIR protein was found at 3 h after ischemia (O2 and glucose deprivation), and thereafter the signal disappeared gradually. Relative optical densities of these bands at 3 h and 8 h after ischemia were 166% (P\u003c0.01) and 44% (P\u003c0.01) of the control (0 h), respectively. In contrast, the results of RT-PCR indicated a same expression of CFTR mRNA between 0 h and 4 h after ischemia. Immunohistochemical examination showed that the expression of CFTR proteins on the plasma membrane was most prominent at 3 h after ischemia. However, the plasmalemmal CFTR signal was markedly reduced at 8 h after ischemia. The time-dependent downregulation was partially prevented by co-appllcation of activators for PKA and PKC. Whole-cell recordings showed that cultured neonatal cardiomyocytes responded to cAMP with activation of time-independent, I-V linear currents which contained an anion-selective component sensitive to aCFTR Cl\u003cSUP\u003e-\u003c/SUP\u003e channel blocker but not to a stilbene-derivative conventional Cl\u003cSUP\u003e-\u003c/SUP\u003e channel blocker. This cAMP-activated Cl\u003cSUP\u003e-\u003c/SUP\u003e channel current was found to be enhanced by 3 to 4 h application of ischemic stress. Only blockers effective for the CFTR channel, among various Cl\u003cSUP\u003e-\u003c/SUP\u003e channel blockers tested, aggravated cell injury observed 4 days after 8-h ischemic treatment. In contrast, activation of CFTR by co-application of PKA and PKC activators was found to enhance cell viability after ischemic stress. The ameliorating effect of PKA and PKC activators was completely abolished by CFTR channel blockers, when applied simultaneously. Neither a CFTR inhibitor nor CFTR activators affected ischemic injury when applied prior to or after, but not during, ischemic treatment. Rhythmic contractility of cultured monolayer cardiomyocytes was impaired during ischemic insult. Four days after reoxygenation contractility recovered partially. The post-ischemic recovery of contractility became perfect by CFTR activators applied during ischemic treatment, whereas this was abolished by a CFTR channel blocker. Taken together, it is concluded that expression of CFTR Cl\u003cSUP\u003e-\u003c/SUP\u003e channel on plasma membrane is transiently enhanced under glucose-free hypoxic conditions, and also that activation of CFTR Cl\u003cSUP\u003e-\u003c/SUP\u003e channels under ischemic conditions may play a crucial role in protection against injury in cardiomyocytes subjected to ischemic stress. 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