Kirschbaum B J, Kucher H B, Termin A, Kelly A M, Pette D
Faculty of Biology, University of Konstanz, Federal Republic of Germany.
J Biol Chem. 1990 Aug 15;265(23):13974-80.
This study investigates effects of chronic low frequency stimulation (CLFS) on myosin heavy (MHC) and light chain (MLC) expression in fast-twitch muscles in hypothyroid, euthyroid, and hyperthyroid rats. The changes at both the mRNA and protein level indicated antagonistic effects of thyroid hormone and CLFS: under euthyroid conditions, CLFS mainly elicited a MHCIIb----MCHIId----MHCIIa transition. Whereas CLFS did not induce the slow MHCI in the euthyroid state, this isoform was present in the hypothyroid state and was further enhanced with CLFS indicating the suppressive effect of thyroid hormone to be stronger than the inductive influence of CLFS. Hyperthyroidism alone suppressed the expression MHCIIa and enhanced a MHCIId to MHCIIb transition. This shift to the faster MHC isoforms was only partially counteracted by CLFS. Thus, it appeared that thyroid hormone had a graded suppressive effect on the expression of MHC isoforms in the order MHCIId less than MHCIIa less than MHCI. Elevated neuromuscular activity partially counteracted these hormone effects. Changes in MLC mRNAs were consistent with those in the MHC pattern, i.e. increases or decreases in MHCIIb led to corresponding changes in the expression of MLC3f. A similar relationship existed for the slow MHCI and the slow MLC isoforms.
本研究调查了慢性低频刺激(CLFS)对甲状腺功能减退、甲状腺功能正常和甲状腺功能亢进大鼠快肌中肌球蛋白重链(MHC)和轻链(MLC)表达的影响。mRNA和蛋白质水平的变化表明甲状腺激素和CLFS具有拮抗作用:在甲状腺功能正常的情况下,CLFS主要引起MHCIIb----MCHIId----MHCIIa转变。虽然CLFS在甲状腺功能正常状态下不会诱导慢肌型MHCI,但这种异构体在甲状腺功能减退状态下存在,并且随着CLFS进一步增强,表明甲状腺激素的抑制作用强于CLFS的诱导作用。单独的甲状腺功能亢进会抑制MHCIIa的表达,并增强MHCII d到MHCIIb的转变。向更快的MHC异构体的这种转变仅被CLFS部分抵消。因此,似乎甲状腺激素对MHC异构体的表达具有分级抑制作用,顺序为MHCII d<MHCIIa<MHCI。神经肌肉活动的增加部分抵消了这些激素的作用。MLC mRNA的变化与MHC模式中的变化一致,即MHCIIb的增加或减少导致MLC3f表达的相应变化。慢肌型MHCI和慢肌型MLC异构体之间也存在类似的关系。