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1.

001-es BibID:BIBFORM120025
035-os BibID:(Scopus)85190380483 (WoS)001200847200001
Első szerző:Csemer Andrea (molekuláris biológus)
Cím:Pharmacological Activation of Piezo1 Channels Enhances Astrocyte-Neuron Communication via NMDA Receptors in the Murine Neocortex / Andrea Csemer, Cintia Sokvári, Baneen Maamrah, László Szabó, Kristóf Korpás, Krisztina Pocsai, Balázs Pál
Dátum:2024
ISSN:1422-0067
Megjegyzések:The Piezo1 mechanosensitive ion channel is abundant on several elements of the central nervous system including astrocytes. It has been already demonstrated that activation of these channels is able to elicit calcium waves on astrocytes, which contributes to the release of gliotransmitters. Astrocyte- and N-methyl-D-aspartate (NMDA) receptor-dependent slow inward currents (SICs) are hallmarks of astrocyte?neuron communication. These currents are triggered by glutamate released as gliotransmitter, which in turn activates neuronal NMDA receptors responsible for this inward current having slower kinetics than any synaptic events. In this project, we aimed to investigate whether Piezo1 activation and inhibition is able to alter spontaneous SIC activity of murine neocortical pyramidal neurons. When the Piezo1 opener Yoda1 was applied, the SIC frequency and the charge transfer by these events in a minute time was significantly increased. These changes were prevented by treating the preparations with the NMDA receptor inhibitor D-AP5. Furthermore, Yoda1 did not alter the spontaneous EPSC frequency and amplitude when SICs were absent. The Piezo1 inhibitor Dooku1 effectively reverted the actions of Yoda1 and decreased the rise time of SICs when applied alone. In conclusion, activation of Piezo1 channels is able to alter astrocyte?neuron communication. Via enhancement of SIC activity, astrocytic Piezo1 channels have the capacity to determine neuronal excitability.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
slow inward current
NMDA receptor
astrocyte
Piezo1
Yoda1
Dooku1
neocortex
pyramidal cell
glutamate
Megjelenés:International Journal Of Molecular Sciences. - 25 : 7 (2024), p. 3994. -
További szerzők:Sokvári Cintia (1995-) Maamrah, Baneen (1994-) (molekuláris biológus) Szabó László (1994-) (molekuláris biológus) Korpás Kristóf Levente (1998-) (orvostanhallgató) Pocsai Krisztina (1978-) (élettanász) Pál Balázs (1975-) (élettanász)
Pályázati támogatás:TKP2020-NKA-04
Egyéb
2020-4.1.1-TKP2020
Egyéb
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2.

001-es BibID:BIBFORM110458
035-os BibID:(Scopus)85152322485 (WoS)000968846200001
Első szerző:Dienes Beatrix (élettanász, molekuláris biológus)
Cím:The Role of the Piezo1 Mechanosensitive Channel in the Musculoskeletal System / Beatrix Dienes, Tamás Bazsó, László Szabó, László Csernoch
Dátum:2023
ISSN:1422-0067
Megjegyzések:Since the recent discovery of the mechanosensitive Piezo1 channels, many studies have addressed the role of the channel in various physiological or even pathological processes of different organs. Although the number of studies on their effects on the musculoskeletal system is constantly increasing, we are still far from a precise understanding. In this review, the knowledge available so far regarding the musculoskeletal system is summarized, reviewing the results achieved in the field of skeletal muscles, bones, joints and cartilage, tendons and ligaments, as well as intervertebral discs.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
mechanosensitive channels
Piezo1
Yoda1
calcium homeostasis
skeletal muscle
cartilage
bone
tendon
ligament
joint
Megjelenés:International Journal Of Molecular Sciences. - 24 : 7 (2023), p. 6513. -
További szerzők:Bazsó Tamás (1974-) (ortopéd sebész) Szabó László (1994-) (molekuláris biológus) Csernoch László (1961-) (élettanász)
Pályázati támogatás:TKP2020-NKA-04
Egyéb
2020-4.1.1-TKP2020
Egyéb
NKFIH K-137600
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM130551
035-os BibID:(WoS)001506005700001
Első szerző:Ganbat, Nyamkhuu (molekuláris biológus)
Cím:Physiological Muscle Function Is Controlled by the Skeletal Endocannabinoid System in Murine Skeletal Muscles / Nyamkhuu Ganbat, Zoltán Singlár, Péter Szentesi, Elena Lilliu, Zoltán Márton Kohler, László Juhász, Anikó Keller-Pintér, Xaver Koenig, Fabio Arturo Iannotti, László Csernoch, Mónika Sztretye
Dátum:2025
ISSN:1661-6596 1422-0067
Megjegyzések:The endocannabinoid system (ECS) is known to regulate crucial bodily functions, including healthy muscle activity. However, its precise roles in normal skeletal muscle function and the development of muscle disorders remain unclear. Previously, we developed a tamoxifen-inducible, skeletal muscle-specific CB1 receptor knockdown (skmCB1-KD) mouse model using the Cre/LoxP system. In this study, we aimed to clarify the mechanisms behind the observed reduction in muscle force generation in these mice. To investigate this, we analyzed calcium dynamics following electrical stimulation-induced muscle fatigue, assessed store-operated calcium entry (SOCE), and performed functional analysis of mitochondrial respiration. Our findings suggest that the reduced muscle performance observed in vivo likely arises from interconnected alterations in ATP production by mitochondria. Moreover, in skmCB1-KD mice, we detected a significant decrease in a component of the respiratory chain (complex IV) and a slowed dissipation of mitochondrial membrane potential upon the addition of an un-coupler (FCCP).
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
skeletal endocannabinoid system
murine skeletal muscle
in vivo muscle force
mitochondrial respiration
calcium homeostasis
store-operated calcium entry
Megjelenés:International Journal Of Molecular Sciences. - 26 : 11 (2025), p. 1-27. -
További szerzők:Singlár Zoltán (1994-) (biotechnológus) Szentesi Péter (1967-) (élettanász) Lilliu, Elena Kohler Zoltán Márton Juhász László Keller-Pintér Anikó Koenig, Xaver Iannotti, Fabio A. Csernoch László (1961-) (élettanász) Sztretye Mónika (1981-) (élettanász, elektrofiziológus)
Pályázati támogatás:FK 142481
OTKA
FK 134684
OTKA
2019-2.1.11-TÉT-2019-00102
Egyéb
TKP2020-NKA-04
Egyéb
TKP2021-EGA-28
Egyéb
FWF 10.55776/P31563
Egyéb
FWF 10.55776/I04649
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM130038
Első szerző:Maamrah, Baneen (molekuláris biológus)
Cím:Chronic Chemogenetic Activation of Astrocytes in the Murine Mesopontine Region Leads to Disturbances in Circadian Activity and Movement / Maamrah Baneen, Pocsai Krisztina, Hoang Bui Minh, Abdelhadi Ali, Al-Khafaji Mustafa Qais, Csemer Andrea, Sokvári Cintia, Szentesi Péter, Pál Balázs
Dátum:2025
ISSN:1661-6596 1422-0067
Megjegyzések:We have previously shown that neuromodulatory actions on astrocytes can elicit metabotropic glutamate- and N-methyl-D-aspartate receptor-dependent tonic changes in excitability in the mesopontine region. Although in vitro experiments explored robust effects, the in vivo significance of our findings remained unknown. In this project, chronic chemogenetic activation of mesopontine astrocytes and its actions on movement, circadian activity, acoustic startle and spatial memory were tested. The control group of young adult male mice where mesopontine astrocytes expressed only the mCherry fluorescent tag was compared to the group expressing the hM3D(Gq) chemogenetic actuator. Chronic chemogenetic astrocyte activation reduced the amplitude of the acoustic startle reflex and increased the locomotion speed in the resting period. Gait alterations were also demonstrated but no change in the spatial memory was explored. As a potential background of these findings, chronic astrocytic activation decreased the cholinergic neuronal number to 54% and reduced the non-cholinergic neuronal number to 76% of the control. In conclusion, chronic astrocytic activation and the consequential decrease in the neuronal number led to disturbances in movement and circadian activity resembling brainstem-related symptoms of progressive supranuclear palsy, raising the possibility that astrocytic overactivation is involved in the pathogenesis of this disease.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
astrocyte
pedunculopontine nucleus
mesopontine region
chemogenetics
acoustic startle
activity cycles
gait
spatial memory
Megjelenés:International Journal Of Molecular Sciences. - 26 : 10 (2025), p. 1-21. -
További szerzők:Pocsai Krisztina (1978-) (élettanász) Hoang, Bui Minh Abdelhadi, Ali Al-Khafaji, Mustafa Qais Muhsin Csemer Andrea (1994-) (molekuláris biológus) Sokvári Cintia (1995-) Szentesi Péter (1967-) (élettanász) Pál Balázs (1975-) (élettanász)
Pályázati támogatás:K146873
OTKA
Stipendium Hungaricum PhD program
Egyéb
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Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM106081
035-os BibID:(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 (1995-) (molekuláris biológus) 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
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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6.

001-es BibID:BIBFORM135271
035-os BibID:(wos)001670630800001
Első szerző:Szabó László (molekuláris biológus)
Cím:The Beneficial Effects of Marine Plant-Derived Compounds on the Musculoskeletal System / Szabó László, Gere Áron, Kovács Zsigmond Máté, Bazsó Tamás, Dienes Beatrix
Dátum:2026
ISSN:1661-6596 1422-0067
Megjegyzések:The skeletal muscle system is particularly susceptible to degenerative and inflammatory processes that threaten mobility, quality of life, and systemic health. Marine plants, including brown, red, and green algae, are valuable yet understudied sources of bioactive compounds with therapeutic potential against skeletal muscle inflammation and degeneration. This narrative review provides the first overview of polyphenols, polysaccharides, carotenoids, and multiminerals derived from marine plants, with a particular focus on their effects on skeletal muscle, bone, and joint tissues. It highlights both the therapeutic potential and the limitations of marine plant-derived bioactive compounds in the musculoskeletal system. The compounds discussed, such as phlorotannins, ulvan, fucoidan, carotenoids, spirulina derivatives, and Aquamin, modulate key signaling pathways, including NF-?B, JAK/STAT3, and the NLRP3 inflammasome. Among these, MAPK emerges as the most consistently affected axis across all compound classes, leading to a reduction in TNF-?, IL-1?, IL-6, and oxidative stress markers. These bioactive compounds have been shown in both in vitro and in vivo models to reduce muscle catabolism, enhance osteoblast differentiation and mineralization, and reduce cartilage inflammation. Despite favorable safety, biocompatibility, and biodegradability profiles, current evidence shows that systemic applications significantly dominate over local delivery, highlighting the untapped potential of localized delivery strategies. Overall, this narrative review underscores the growing importance of marine plant-derived bioactives as promising natural agents for maintaining musculoskeletal integrity and alleviating degenerative disorders.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
marine plant derivatives
anti-inflammatory effects
musculoskeletal system
muscle atrophy
osteoarthritis
Megjelenés:International Journal Of Molecular Sciences. - 27 : 2 (2026), p. 1-21. -
További szerzők:Gere Áron Kovács Zsigmond Máté (1995-) (orvos) Bazsó Tamás (1974-) (ortopéd sebész) Dienes Beatrix (1972-) (élettanász, molekuláris biológus)
Internet cím:Szerző által megadott URL
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Intézményi repozitóriumban (DEA) tárolt változat
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7.

001-es BibID:BIBFORM114566
035-os BibID:(scopus)85170341617 (wos)001061092600001
Első szerző:Szabó László (molekuláris biológus)
Cím:Reduced Expression of Septin7 Hinders Skeletal Muscle Regeneration / Szabó László, Telek Andrea, Fodor János, Dobrosi Nóra, Dócs Klaudia, Hegyi Zoltán, Gönczi Mónika, Csernoch László, Dienes Beatrix
Dátum:2023
ISSN:1422-0067
Megjegyzések:Septins are considered the fourth component of the cytoskeleton with the septin7 isoform playing a critical role in the formation of diffusion barriers in phospholipid bilayers and intra- and extracellular scaffolds. While its importance has already been confirmed in different intracellular processes, very little is known about its role in skeletal muscle. Muscle regeneration was studied in a Sept7 conditional knock-down mouse model to prove the possible role of septin7 in this process. Sterile inflammation in skeletal muscle was induced which was followed by regeneration resulting in the upregulation of septin7 expression. Partial knock-down of Sept7 resulted in an increased number of inflammatory cells and myofibers containing central nuclei. Taken together, our data suggest that partial knock-down of Sept7 hinders the kinetics of muscle regeneration, indicating its crucial role in skeletal muscle functions.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
septin7
skeletal muscle
regeneration
central nuclei
muscle injury
Megjelenés:International Journal Of Molecular Sciences. - 24 : 17 (2023), p. 13536. -
További szerzők:Telek Andrea (1977-) (élettanász) Fodor János (1973-) (élettanász, biotechnológus) Dobrosi Nóra (1981-) (molekuláris biológus) Dócs Klaudia (1989-) (orvos) Hegyi Zoltán (1983-) (molekuláris biológus) Gönczi Mónika (1974-) (élettanász) Csernoch László (1961-) (élettanász) Dienes Beatrix (1972-) (élettanász, molekuláris biológus)
Pályázati támogatás:NKFIH K-137600
Egyéb
TKP2020-NKA-04
Egyéb
2020-4.1.1-TKP2020
Egyéb
TKP2021-EGA-18
Egyéb
Internet cím:Szerző által megadott URL
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Intézményi repozitóriumban (DEA) tárolt változat
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8.

001-es BibID:BIBFORM110527
035-os BibID:(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 (1995-) (molekuláris biológus) 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
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