Korean J Physiol Pharmacol.  2015 May;19(3):283-289. 10.4196/kjpp.2015.19.3.283.

Improvement Characteristics of Bio-active Materials Coated Fabric on Rat Muscular Mitochondria

Affiliations
  • 1Department of Physiology, College of Medicine, Chung-Ang University, Seoul 156-756, Korea. akdongyi01@cau.ac.kr
  • 2Department of Family Medicine, College of Medicine, Chung-Ang University, Seoul 156-756, Korea.
  • 3Research and Development Center, VENTEX Co. Ltd., Seoul 138-220, Korea.

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.

Keyword

Apoptosis; Bio-active materials coated fabric; Mitochondria; Mitophagy; Oxidative respiration

MeSH Terms

Actins
Animals
Antigens, CD95
Apoptosis
Caspase 3
Caspase 9
DNA, Mitochondrial
Mitochondria*
Mitochondrial Degradation
Muscle, Skeletal
Oxygen Consumption
Rats*
Respiration
RNA, Messenger
Actins
Antigens, CD95
Caspase 3
Caspase 9
DNA, Mitochondrial
RNA, Messenger

Figure

  • Fig. 1 Effect of BMCF on the expression of oxygen consumption. V-Con, 0% BMCF group; V-10, 10% BMCF group; V-30, 30% BMCF group. **p<0.01, ***p<0.001.

  • Fig. 2 Effect of BMCF on the expression of mitochondrial DNA copy number. V-Con, 0% BMCF group; V-10, 10% BMCF group; V-30, 30% BMCF group. *p<0.05, **p<0.01.

  • Fig. 3 Effect of BMCF on the expression of oxygen consumption to mitochondrial DNA copy number through 4 weeks. V-Con, 0% BMCF group (n=26); V-10, 10% BMCF (n=19); V-30, 30% BMCF group (n=27). ***p<0.001.

  • Fig. 4 PCR amplification of the cDNA with B-cell lymphoma 2 gene (Bcl-2), Bcl-2-associated X protein (Bax), PTEN-induced putative kinase 1 (PINK1), Peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α), beta-actin (β-actin) and 18S ribosomal RNA (18S) from rat subtrapezial muscle.

  • Fig. 5 Effect of BMCF on the mRNA expressions of caspase 9 (CASP9), caspase 3 (CASP3), Bcl-2-associated X protein (Bax), B-cell lymphoma 2 gene (Bcl-2), Fas receptor (FasR) and beta-actin (β-actin). (A) CASP9, (B) CASP3, (C) Bax, (D) Bcl-2, (E) FasR, (F) β-actin. *p<0.05, **p<0.01, ***p<0.001.


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