Improvement Characteristics of Bio-active Materials Coated Fabric on Rat Muscular Mitochondria.
10.4196/kjpp.2015.19.3.283
- Author:
Donghee LEE
1
;
Young Won KIM
;
Jung Ha KIM
;
Misuk YANG
;
Hyemi BAE
;
Inja LIM
;
Hyoweon BANG
;
Kyung Chan GO
;
Gwang Wung YANG
;
Yong Hwan RHO
;
Hyo Suk PARK
;
Eun Ho PARK
;
Jae Hong KO
Author Information
1. Department of Physiology, College of Medicine, Chung-Ang University, Seoul 156-756, Korea. akdongyi01@cau.ac.kr
- Publication Type:Original Article
- Keywords:
Apoptosis;
Bio-active materials coated fabric;
Mitochondria;
Mitophagy;
Oxidative respiration
- MeSH:
Actins;
Animals;
Antigens, CD95;
Apoptosis;
Caspase 3;
Caspase 9;
DNA, Mitochondrial;
Mitochondria*;
Mitochondrial Degradation;
Muscle, Skeletal;
Oxygen Consumption;
Rats*;
Respiration;
RNA, Messenger
- From:The Korean Journal of Physiology and Pharmacology
2015;19(3):283-289
- CountryRepublic of Korea
- Language:English
-
Abstract:
This study surveys the improvement characteristics in old-aged muscular mitochondria by bio-active materials coated fabric (BMCF). To observe the effects, the fabric (10 and 30%) was worn to old-aged rat then the oxygen consumption efficiency and copy numbers of mitochondria, and mRNA expression of apoptosis- and mitophagy-related genes were verified. By wearing the BMCF, the oxidative respiration significantly increased when using the 30% materials coated fabric. The mitochondrial DNA copy number significantly decreased and subsequently recovered in a dose-dependent manner. The respiratory control ratio to mitochondrial DNA copy number showed a dose-dependent increment. As times passed, Bax, caspase 9, PGC-1alpha and beta-actin increased, and Bcl-2 decreased in a dose-dependent manner. However, the BMCF can be seen to have had no effect on Fas receptor. PINK1 expression did not change considerably and was inclined to decrease in control group, but the expression was down-regulated then subsequently increased with the use of the BMCF in a dose-dependent manner. Caspase 3 increased and subsequently decreased in a dose-dependent manner. These results suggest that the BMCF invigorates mitophagy and improves mitochondrial oxidative respiration in skeletal muscle, and in early stage of apoptosis induced by the BMCF is not related to extrinsic death-receptor mediated but mitochondria-mediated signaling pathway.
