Calcium-induced alteration of mitochondrial morphology and mitochondrial-endoplasmic reticulum contacts in rat brown adipocytes.
Calcium-induced alteration of mitochondrial morphology and mitochondrial-endoplasmic reticulum contacts in rat brown adipocytes.
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DOI:
10.4081/ejh.2014.2377
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发表时间:
2014-09-09
期刊:
影响因子:
--
通讯作者:
Korac A
中科院分区:
文献类型:
--
作者:
Golic I;Velickovic K;Markelic M;Stancic A;Jankovic A;Vucetic M;Otasevic V;Buzadzic B;Korac B;Korac A
Mitochondria are key organelles maintaining cellular bioenergetics and integrity, and their regulation of [Ca2+]i homeostasis has been investigated in many cell types. We investigated the short-term Ca-SANDOZ® treatment on brown adipocyte mitochondria, using imaging and molecular biology techniques. Two-month-old male Wistar rats were divided into two groups: Ca-SANDOZ® drinking or tap water (control) drinking for three days. Alizarin Red S staining showed increased Ca2+ level in the brown adipocytes of treated rats, and potassium pyroantimonate staining localized electron-dense regions in the cytoplasm, mitochondria and around lipid droplets. Ca-SANDOZ® decreased mitochondrial number, but increased their size and mitochondrial cristae volume. Transmission electron microscopy revealed numerous enlarged and fusioned-like mitochondria in the Ca-SANDOZ® treated group compared to the control, and megamitochondria in some brown adipocytes. The Ca2+ diet affected mitochondrial fusion as mitofusin 1 (MFN1) and mitofusin 2 (MFN2) were increased, and mitochondrial fission as dynamin related protein 1 (DRP1) was decreased. Confocal microscopy showed a higher colocalization rate between functional mitochondria and endoplasmic reticulum (ER). The level of uncoupling protein-1 (UCP1) was elevated, which was confirmed by immunohistochemistry and Western blot analysis. These results suggest that Ca-SANDOZ® stimulates mitochondrial fusion, increases mitochondrial-ER contacts and the thermogenic capacity of brown adipocytes.
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影响因子:
64.5
作者:
Cárdenas C;Miller RA;Smith I;Bui T;Molgó J;Müller M;Vais H;Cheung KH;Yang J;Parker I;Thompson CB;Birnbaum MJ;Hallows KR;Foskett JK
通讯作者:
Foskett JK
影响因子:
4
作者:
Hayato, Ryotaro;Higure, Yoko;Kuba, Kenji
通讯作者:
Kuba, Kenji
DOI:
10.1083/jcb.200211046
发表时间:
2003-01-20
期刊:
The Journal of cell biology
影响因子:
--
作者:
Chen H;Detmer SA;Ewald AJ;Griffin EE;Fraser SE;Chan DC
通讯作者:
Chan DC
影响因子:
64.5
作者:
HAJNOCZKY, G;ROBBGASPERS, LD;THOMAS, AP
通讯作者:
THOMAS, AP
DOI:
10.1111/j.1432-1033.1984.tb08173.x
发表时间:
1984-01-01
期刊:
EUROPEAN JOURNAL OF BIOCHEMISTRY
影响因子:
--
作者:
CONNOLLY, E;NANBERG, E;NEDERGAARD, J
通讯作者:
NEDERGAARD, J