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β2-Adrenoceptor is involved in connective tissue remodeling in regenerating muscles by decreasing the activity of
Meiricris T Silva1, Tábata L Nascimento1, Marcelo G Pereira1
1Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, Av. Prof. Lineu Prestes 2415, 05508-000, São Paulo, SP, Brazil.
Abstract:
We investigated the role of β2-adrenoceptors in the connective tissue remodeling of regenerating muscles from β2-adrenoceptor knockout (β2KO) mice. Tibialis anterior muscles from β2KO mice were cryolesioned and analyzed after 3, 10, and 21 days. Regenerating muscles from β2KO mice showed a significant increase in the area density of the connective tissue and in the amount of collagen at 10 days compared with wild-type (WT) mice. A greater increase occurred in the expression levels of collagen I, III, and IV in regenerating muscles from β2KO mice evaluated at 10 days compared with WT mice; this increase continued at 21 days, except for collagen III. Matrix metalloproteinase (MMP-2) activity increased to a similar extent in regenerating muscles from both β2KO and WT mice at 3 and 10 days. This was also the case for MMP-9 activity in regenerating muscles from both β2KO and WT mice at 3 days; however, at 10 days post-cryolesion, this activity returned to baseline levels only in WT mice. MMP-3 activity was unaltered in regenerating muscles at 10 days. mRNA levels of tumor necrosis factor-α increased in regenerating muscles from WT and β2KO mice at 3 days and, at 10 days post-cryolesion, returned to baseline only in WT mice. mRNA levels of interleukin-6 increased in muscles from WT mice at 3 days post-cryolesion and returned to baseline at 10 days post-cryolesion but were unchanged in β2KO mice. Our results suggest that the β2-adrenoceptor contributes to collagen remodeling during muscle regeneration by decreasing MMP-9 activity.
Insights
The beta-2 adrenoceptor (β2AR) plays a crucial role in muscle regeneration by regulating connective tissue remodeling. Absence of β2AR in knockout mice leads to increased collagen deposition and altered matrix metalloproteinase activity during muscle repair.
Area of Science:
- Muscle regeneration
- Connective tissue remodeling
- Adrenergic signaling
Background:
- Skeletal muscle regeneration involves complex processes including inflammation, proliferation, and remodeling.
- Connective tissue remodeling, particularly collagen deposition, is critical for restoring muscle function.
- The role of specific adrenergic receptors, like β2AR, in modulating these regenerative processes remains incompletely understood.
Purpose of the Study:
- To investigate the role of β2-adrenoceptors (β2AR) in connective tissue remodeling during skeletal muscle regeneration.
- To compare the regenerative capacity and molecular changes in β2AR knockout (β2KO) mice versus wild-type (WT) mice following cryoinjury.
Main Methods:
- Cryoinjury was induced in the tibialis anterior muscles of β2KO and WT mice.
- Muscle tissues were analyzed at 3, 10, and 21 days post-injury.
- Analysis included assessment of connective tissue area, collagen content, gene expression (collagens, TNF-α, IL-6), and matrix metalloproteinase (MMP) activity (MMP-2, -3, -9).
Main Results:
- β2KO mice exhibited significantly increased connective tissue and collagen deposition at 10 days post-injury compared to WT mice.
- Collagen I, III, and IV expression was elevated in β2KO mice, persisting for collagen I and IV at 21 days.
- While MMP-2 activity was similar, MMP-9 activity and TNF-α mRNA levels returned to baseline only in WT mice by 10 days, suggesting impaired resolution in β2KO mice.
- Interleukin-6 mRNA levels were unchanged in β2KO mice at 3 days, unlike in WT mice.
Conclusions:
- β2-adrenoceptors are essential for proper connective tissue remodeling during muscle regeneration.
- The absence of β2AR leads to excessive collagen accumulation and delayed resolution of inflammatory markers.
- β2AR signaling appears to modulate muscle repair by regulating MMP-9 activity, thereby influencing the balance of matrix deposition and degradation.
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