Heat stress increases myonuclear number and fiber size via satellite cell activation in rat regenerating soleus fibers

Oishi, Yasuharu; Hayashida, Mari; Tsukiashi, Shinsuke; Taniguchi, Kohachi; Kami, Katsuya; Roy, Roland R.; Ohira, Yoshinobu

doi:10.1152/japplphysiol.91651.2008

Cited by 52 publications

(55 citation statements)

References 58 publications

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“…6). This novel finding might help explain why repeated heat therapy application facilitates regeneration of injured skeletal muscle (50,72). Individuals exposed to LBH had higher mRNA levels of CCL2 and CX3CL1 relative to the control group (Fig.…”

Section: Skeletal Muscle Angiogenic Signalingmentioning

confidence: 80%

Heat therapy promotes the expression of angiogenic regulators in human skeletal muscle

Kuhlenhoelter

Kim

Neff

et al. 2016

American Journal of Physiology-Regulatory, Integrative and Comp

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Heat therapy has been shown to promote capillary growth in skeletal muscle and in the heart in several animal models, but the effects of this therapy on angiogenic signaling in humans are unknown. We evaluated the acute effect of lower body heating (LBH) and unilateral thigh heating (TH) on the expression of angiogenic regulators and heat shock proteins (HSPs) in healthy young individuals. Exposure to LBH ( n = 18) increased core temperature (Tc) from 36.9 ± 0.1 to 37.4 ± 0.1°C ( P < 0.01) and average leg skin temperature (Tleg) from 33.1 ± 0.1 to 39.6 ± 0.1°C ( P < 0.01), but did not alter the levels of circulating angiogenic cytokines and bone marrow-derived proangiogenic cells (CD34+CD133+). In skeletal muscle, the change in mRNA expression from baseline of vascular endothelial growth factor (VEGF), angiopoietin 2 (ANGPT2), chemokines CCL2 and CX3CL1, platelet factor-4 (PF4), and several members of the HSP family was higher 30 min after the intervention in the individuals exposed to LBH ( n = 11) compared with the control group ( n = 12). LBH also reduced the expression of transcription factor FOXO1 ( P = 0.03). Exposure to TH ( n = 14) increased Tleg from 32.8 ± 0.2 to 40.3 ± 0.1°C ( P < 0.05) but Tc remained unaltered (36.8 ± 0.1°C at baseline and 36.9 ± 0.1°C at 90 min). This intervention upregulated the expression of VEGF, ANGPT1, ANGPT2, CCL2, and HSPs in skeletal muscle but did not affect the levels of CX3CL1, FOXO-1, and PF4. These findings suggest that both LBH and TH increase the expression of factors associated with capillary growth in human skeletal muscle.

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Section: Skeletal Muscle Angiogenic Signalingmentioning

confidence: 80%

Heat therapy promotes the expression of angiogenic regulators in human skeletal muscle

Kuhlenhoelter

Kim

Neff

et al. 2016

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Heat stress was performed according to a method reported in a previous study (13). The lower half of the body of the rat was immersed in hot water at 42 °C for 30 min under anesthesia (intraperitoneal injection of 50 mg/kg sodium pentobarbital).…”

Section: Animals and Heat Stressmentioning

confidence: 99%

Heat stress attenuates skeletal muscle atrophy of extensor digitorum longus in streptozotocin-induced diabetic rats

Nonaka¹,

Une²,

Akiyama³

2015

Acta Physiologica Hungarica

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To investigate whether heat stress attenuates skeletal muscle atrophy of the extensor digitorum longus (EDL) muscle in streptozotocin-induced diabetic rats, 12-week-old male Wistar rats were randomly assigned to four groups (n = 6 per group): control (Con), heat stress (HS), diabetes mellitus (DM), and diabetes mellitus/heat stress (DM + HS). Diabetes was induced by intraperitoneal injection of streptozotocin (50 mg/kg). Heat stress was induced in the HS and DM + HS groups by immersion of the lower half of the body in hot water at 42 °C for 30 min; it was initiated 7 days after injection of streptozotocin, and was performed once a day, five times a week for 3 weeks. The muscle fiber cross-sectional area of EDL muscles from diabetic and non-diabetic rats was determined; heat stress protein (HSP) 72 and HSP25 expression levels were also analyzed by western blotting. Diabetes-induced muscle fiber atrophy was attenuated upon heat stress treatment in diabetic rats. HSP72 and HSP25 expression was upregulated in the DM + HS group compared with the DM group. Our findings suggest that heat stress attenuates atrophy of the EDL muscle by upregulating HSP72 and HSP25 expression.Keywords: extensor digitorum longus muscle, heat stress, HSP72, HSP25, skeletal muscle atrophy, streptozotocin-induced diabetes Diabetes mellitus (DM) induces skeletal muscle atrophy (7, 19) and decreases muscle strength (7, 9). Consequently, patients with diabetes have a higher risk of falls because of reduced muscle strength (8, 16) and DM-induced-muscle atrophy. Where DM induces skeletal muscle atrophy, fast-twitch fibers are prone to greater atrophy than are slow-twitch fibers (1). Fast-twitch fibers are responsible for high force/power/speed production and maintaining physical balance during postural perturbation. Hence, atrophy of fast-twitch muscle increases the risk of falling in DM patients. Therefore, an efficient strategy is required to attenuate muscle atrophy in order to reduce the risk of falls in DM patients. Heat shock proteins (HSPs) have a protective effect on muscle atrophy. Senf et al. reported that HSP70 overexpression prevented rat soleus muscle fiber atrophy induced by hind limb immobilization (18). Furthermore, overexpression of HSP27 also prevented muscle fiber atrophy of the soleus muscle induced by disuse in rats (5). HSPs are expressed in response to several types of stress such as heat (14, 15) and exercise (12). Exercise increased HSP72 expression (2) and attenuated skeletal muscle fiber atrophy (3) in streptozotocin

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“…When activated, these proliferate, differentiate, and fuse to form myotubes, in which the nuclei are positioned at the center of the syncytium (10,13). The centrally nucleated myofibers may be observed from around 3 days after muscle injury induced by bupivacaine and remain visible up to 14 days (4,16,28). Next, the newly formed myofibers grow continuously until they reach the size of mature fibers.…”

mentioning

confidence: 99%

“…During maturation, the central located nuclei move to the periphery of the myofiber. The process of soleus muscle regeneration following bupivacaine injection may be accelerated, such as by the application of heat stress (28). The beneficial effect of heat stress on muscle regeneration is associated with the satellite cells, which are activated in the damaged site (28).…”

mentioning

confidence: 99%

PEDF-derived peptide promotes skeletal muscle regeneration through its mitogenic effect on muscle progenitor cells

Chiang

Chen

et al. 2015

American Journal of Physiology-Cell Physiology

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In response injury, intrinsic repair mechanisms are activated in skeletal muscle to replace the damaged muscle fibers with new muscle fibers. The regeneration process starts with the proliferation of satellite cells to give rise to myoblasts, which subsequently differentiate terminally into myofibers. Here, we investigated the promotion effect of pigment epithelial-derived factor (PEDF) on muscle regeneration. We report that PEDF and a synthetic PEDF-derived short peptide (PSP; residues Ser(93)-Leu(112)) induce satellite cell proliferation in vitro and promote muscle regeneration in vivo. Extensively, soleus muscle necrosis was induced in rats by bupivacaine, and an injectable alginate gel was used to release the PSP in the injured muscle. PSP delivery was found to stimulate satellite cell proliferation in damaged muscle and enhance the growth of regenerating myofibers, with complete regeneration of normal muscle mass by 2 wk. In cell culture, PEDF/PSP stimulated C2C12 myoblast proliferation, together with a rise in cyclin D1 expression. PEDF induced the phosphorylation of ERK1/2, Akt, and STAT3 in C2C12 myoblasts. Blocking the activity of ERK, Akt, or STAT3 with pharmacological inhibitors attenuated the effects of PEDF/PSP on the induction of C2C12 cell proliferation and cyclin D1 expression. Moreover, 5-bromo-2'-deoxyuridine pulse-labeling demonstrated that PEDF/PSP stimulated primary rat satellite cell proliferation in myofibers in vitro. In summary, we report for the first time that PSP is capable of promoting the regeneration of skeletal muscle. The signaling mechanism involves the ERK, AKT, and STAT3 pathways. These results show the potential utility of this PEDF peptide for muscle regeneration.

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Heat stress increases myonuclear number and fiber size via satellite cell activation in rat regenerating soleus fibers

Cited by 52 publications

References 58 publications

Heat therapy promotes the expression of angiogenic regulators in human skeletal muscle

Heat therapy promotes the expression of angiogenic regulators in human skeletal muscle

Heat stress attenuates skeletal muscle atrophy of extensor digitorum longus in streptozotocin-induced diabetic rats

PEDF-derived peptide promotes skeletal muscle regeneration through its mitogenic effect on muscle progenitor cells

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