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001-es BibID:BIBFORM106081
035-os BibID:(cikkazonosító)15653 (WoS)000901106200001 (Scopus)85144543882 (PubMed)36555292
Első szerző:Singlár Zoltán (biotechnológus)
Cím:Genetic Manipulation of CB1 Cannabinoid Receptors Reveals a Role in Maintaining Proper Skeletal Muscle Morphology and Function in Mice / Singlár Zoltán, Ganbat Nyamkhuu, Szentesi Péter, Osgonsandag Nomin, Szabó László, Telek Andrea, Fodor János, Dienes Beatrix, Gönczi Mónika, Csernoch László, Sztretye Mónika
Dátum:2022
ISSN:1422-0067
Megjegyzések:The endocannabinoid system (ECS) refers to a widespread signaling system and its alteration is implicated in a growing number of human diseases. Cannabinoid receptors (CBRs) are highly expressed in the central nervous system and many peripheral tissues. Evidence suggests that CB1Rs are expressed in human and murine skeletal muscle mainly in the cell membrane, but a subpopulation is present also in the mitochondria. However, very little is known about the latter population. To date, the connection between the function of CB1Rs and the regulation of intracellular Ca2+ signaling has not been investigated yet. Tamoxifen-inducible skeletal muscle-specific conditional CB1 knock-down (skmCB1-KD, hereafter referred to as Cre(+/-)) mice were used in this study for functional and morphological analysis. After confirming CB1R down-regulation on the mRNA and protein level, we performed in vitro muscle force measurements and found that peak twitch, tetanus, and fatigue were decreased significantly in Cre(+/-) mice. Resting intracellular calcium concentration, voltage dependence of the calcium transients as well as the activity dependent mitochondrial calcium uptake were essentially unaltered by Cnr1 gene manipulation. Nevertheless, we found striking differences in the ultrastructural architecture of the mitochondrial network of muscle tissue from the Cre(+/-) mice. Our results suggest a role of CB1Rs in maintaining physiological muscle function and morphology. Targeting ECS could be a potential tool in certain diseases, including muscular dystrophies where increased endocannabinoid levels have already been described.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
endocannabinoid system (ECS)
cannabinoid receptor of type 1 (CBR1)
skeletal muscle force
contractility
excitation-contraction coupling (ECC)
mitochondria
intracellular calcium
Megjelenés:International Journal Of Molecular Sciences. - 23 : 24 (2022), p. 1-21. -
További szerzők:Ganbat, Nyamkhuu Szentesi Péter (1967-) (élettanász) Osgonsandag, Nomin Szabó László (1994-) (molekuláris biológus) Telek Andrea (1977-) (élettanász) Fodor János (1973-) (élettanász, biotechnológus) Dienes Beatrix (1972-) (élettanász, molekuláris biológus) Gönczi Mónika (1974-) (élettanász) Csernoch László (1961-) (élettanász) Sztretye Mónika (1981-) (élettanász, elektrofiziológus)
Pályázati támogatás:NKFIH-FK-142481
Egyéb
NKFIH K-137600
Egyéb
NKFIH 2019-2.1.11-TÉT-2019-00063
Egyéb
ÚNKP-22-3-II-DE-239
Egyéb
EFOP-3.6.3-VEKOP-16-2017-00009
EFOP
TKP2021-EGA-18
Egyéb
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2.

001-es BibID:BIBFORM110527
035-os BibID:(cikkazonosító)6933 (Scopus)85156172024 (WoS)000979332900001
Első szerző:Sztretye Mónika (élettanász, elektrofiziológus)
Cím:Unravelling the Effects of Syndecan-4 Knockdown on Skeletal Muscle Functions / Mónika Sztretye, Zoltán Singlár, Nyamkhuu Ganbat, Dána Al-Gaadi, Kitti Szabó, Zoltán Márton Köhler, László Dux, Anikó Keller-Pintér, László Csernoch, Péter Szentesi
Dátum:2023
ISSN:1422-0067
Megjegyzések:The remodelling of the extracellular matrix plays an important role in skeletal muscle development and regeneration. Syndecan-4 is a cell surface proteoglycan crucial for muscle differentiation. Syndecan-4?/? mice have been reported to be unable to regenerate following muscle damage. To investigate the consequences of the decreased expression of Syndecan-4, we have studied the in vivo and in vitro muscle performance and the excitation?contraction coupling machinery in young and aged Syndecan-4+/? (SDC4) mice. In vivo grip force was decreased significantly as well as the average and maximal speed of voluntary running in SDC4 mice, regardless of their age. The maximal in vitro twitch force was reduced in both EDL and soleus muscles from young and aged SDC4 mice. Ca2+ release from the sarcoplasmic reticulum decreased significantly in the FDB fibres of young SDC4 mice, while its voltage dependence was unchanged regardless of age. These findings were present in muscles from young and aged mice as well. On C2C12 murine skeletal muscle cells, we have also found altered calcium homeostasis upon Syndecan-4 silencing. The decreased expression of Syndecan-4 leads to reduced skeletal muscle performance in mice and altered motility in C2C12 myoblasts via altered calcium homeostasis. The altered muscle force performance develops at an early age and is maintained throughout the life course of the animal until old age.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Syndecan-4
skeletal muscle
force
calcium homeostasis
aging
Megjelenés:International Journal Of Molecular Sciences. - 24 : 8 (2023), p. 6933. -
További szerzők:Singlár Zoltán (1994-) (biotechnológus) Ganbat, Nyamkhuu Al-Gaadi, Dana (1991-) Szabó Kitti Köhler Zoltán Márton Dux László Keller-Pintér Anikó Csernoch László (1961-) (élettanász) Szentesi Péter (1967-) (élettanász)
Pályázati támogatás:NKFIH K137600
Egyéb
TKP2020-NKA-04
Egyéb
NKFIH FK-142481
Egyéb
NKFIH FK134684
Egyéb
TKP2021-EGA-28
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
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