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Article: Maintenance of subsynaptic myonuclei number is not driven by neural input.

Ruiz, Lloyd P / Macpherson, Peter C / Brooks, Susan V

2023 Volume 14, Page(s) 1266950

Abstract: The development and maintenance of neuromuscular junctions (NMJ) are supported by a specialized population of myonuclei that are referred to as the subsynaptic myonuclei (SSM). The relationship between the number of SSM and the integrity of the NMJ as ... ...

Abstract	The development and maintenance of neuromuscular junctions (NMJ) are supported by a specialized population of myonuclei that are referred to as the subsynaptic myonuclei (SSM). The relationship between the number of SSM and the integrity of the NMJ as well as the impact of a loss of innervation on SSM remain unclear. This study aimed to clarify these associations by simultaneously analyzing SSM counts and NMJ innervation status in three distinct mouse models of acute and chronic NMJ disruption. SSM were identified using fluorescent immunohistochemistry for Nesprin1 expression, which is highly enriched in SSM, along with anatomical location beneath the muscle fiber motor endplate. Acute denervation, induced by surgical nerve transection, did not affect SSM number after 7 days. Additionally, no significant changes in SSM number were observed during normal aging or in mice with chronic oxidative stress (
Language	English
Publishing date	2023-09-26
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2023.1266950
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Article ; Online: Eccentric Exercise as a Potent Prescription for Muscle Weakness After Joint Injury.

Lepley, Lindsey K / Stoneback, Luke / Macpherson, Peter C D / Butterfield, Timothy A

Exercise and sport sciences reviews

2023 Volume 51, Issue 3, Page(s) 109–116

Abstract: Lengthening contractions (i.e., eccentric contractions) are capable of uniquely triggering the nervous system and signaling pathways to promote tissue health/growth. This mode of exercise may be particularly potent for patients suffering from muscle ... ...

Abstract	Lengthening contractions (i.e., eccentric contractions) are capable of uniquely triggering the nervous system and signaling pathways to promote tissue health/growth. This mode of exercise may be particularly potent for patients suffering from muscle weakness after joint injury. Here we provide a novel framework for eccentric exercise as a safe, effective mode of exercise prescription for muscle recovery.
MeSH term(s)	Humans ; Exercise/physiology ; Muscle Contraction/physiology ; Muscle Weakness ; Exercise Therapy ; Signal Transduction ; Muscle, Skeletal/physiology
Language	English
Publishing date	2023-04-24
Publishing country	United States
Document type	Journal Article
ZDB-ID	187040-3
ISSN	1538-3008 ; 0091-6331
ISSN (online)	1538-3008
ISSN	0091-6331
DOI	10.1249/JES.0000000000000319
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Article: Decoding muscle-resident Schwann cell dynamics during neuromuscular junction remodeling.

Guzman, Steve D / Abu-Mahfouz, Ahmad / Davis, Carol S / Ruiz, Lloyd P / Macpherson, Peter C / Brooks, Susan V

bioRxiv : the preprint server for biology

2023

Abstract: Understanding neuromuscular junction (NMJ) repair mechanisms is essential for addressing degenerative neuromuscular conditions. Here, we focus on the role of muscle-resident Schwann cells in NMJ reinnervation. In ... ...

Abstract	Understanding neuromuscular junction (NMJ) repair mechanisms is essential for addressing degenerative neuromuscular conditions. Here, we focus on the role of muscle-resident Schwann cells in NMJ reinnervation. In young
Language	English
Publishing date	2023-10-07
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.10.06.561193
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Article ; Online: Older mice show decreased regeneration of neuromuscular junctions following lengthening contraction-induced injury.

Paul, Thomas A / Macpherson, Peter C / Janetzke, Tara L / Davis, Carol S / Jackson, Malcolm J / McArdle, Anne / Brooks, Susan V

GeroScience

2023 Volume 45, Issue 3, Page(s) 1899–1912

Abstract: Progressive muscle atrophy and loss of muscle strength associated with old age have been well documented. Although age-associated impairments in skeletal muscle regeneration following injury have been demonstrated, less is known about whether aging ... ...

Abstract	Progressive muscle atrophy and loss of muscle strength associated with old age have been well documented. Although age-associated impairments in skeletal muscle regeneration following injury have been demonstrated, less is known about whether aging impacts the regenerative response of neuromuscular junctions (NMJ) following contraction-induced injury. Reduced ability of NMJs to regenerate could lead to increased numbers of denervated muscle fibers and therefore play a contributing role to age-related sarcopenia. To investigate the relationship between age and NMJ regeneration following injury, extensor digitorum longus (EDL) muscles of middle-aged (18-19 months) and old mice (27-28 months) were subjected to a protocol of lengthening contractions (LC) that resulted in an acute force deficit of ~55% as well as functional and histological evidence of a similar magnitude of injury 3 days post LCs that was not different between age groups. After 28 days, the architecture and innervation of the NMJs were evaluated. The numbers of fragmented endplates increased and of fully innervated NMJs decreased post-injury for the muscle of both middle-aged and old mice and for contralateral uninjured muscles of old compared with uninjured muscles of middle-aged controls. Thus, the diminished ability of the skeletal muscle of old mice to recover following injury may be due in part to an age-related decrease in the ability to regenerate NMJs in injured muscles. The impaired ability to regenerate NMJs may be a triggering factor for degenerative changes at the NMJ contributing to muscle fiber weakness and loss in old age.
MeSH term(s)	Mice ; Animals ; Muscle Contraction ; Neuromuscular Junction ; Muscle Fibers, Skeletal ; Muscle, Skeletal/pathology ; Regeneration
Language	English
Publishing date	2023-03-23
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2886586-8
ISSN	2509-2723 ; 2509-2715
ISSN (online)	2509-2723
ISSN	2509-2715
DOI	10.1007/s11357-023-00774-w
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Article: High-Resolution Spatial Transcriptomic Atlas of Mouse Soleus Muscle: Unveiling Single Cell and Subcellular Heterogeneity in Health and Denervation.

Hsu, Jer-En / Ruiz, Lloyd / Hwang, Yongha / Guzman, Steve / Cho, Chun-Seok / Cheng, Weiqiu / Si, Yichen / Macpherson, Peter / Schrank, Mitchell / Jun, Goo / Kang, Hyun-Min / Kim, Myungjin / Brooks, Susan / Lee, Jun Hee

bioRxiv : the preprint server for biology

2024

Abstract: Skeletal muscle is essential for both movement and metabolic processes, characterized by a complex and ordered structure. Despite its importance, a detailed spatial map of gene expression within muscle tissue has been challenging to achieve due to the ... ...

Abstract	Skeletal muscle is essential for both movement and metabolic processes, characterized by a complex and ordered structure. Despite its importance, a detailed spatial map of gene expression within muscle tissue has been challenging to achieve due to the limitations of existing technologies, which struggle to provide high-resolution views. In this study, we leverage the Seq-Scope technique, an innovative method that allows for the observation of the entire transcriptome at an unprecedented submicron spatial resolution. By applying this technique to the mouse soleus muscle, we analyze and compare the gene expression profiles in both healthy conditions and following denervation, a process that mimics aspects of muscle aging. Our approach reveals detailed characteristics of muscle fibers, other cell types present within the muscle, and specific subcellular structures such as the postsynaptic nuclei at neuromuscular junctions, hybrid muscle fibers, and areas of localized expression of genes responsive to muscle injury, along with their histological context. The findings of this research significantly enhance our understanding of the diversity within the muscle cell transcriptome and its variation in response to denervation, a key factor in the decline of muscle function with age. This breakthrough in spatial transcriptomics not only deepens our knowledge of muscle biology but also sets the stage for the development of new therapeutic strategies aimed at mitigating the effects of aging on muscle health, thereby offering a more comprehensive insight into the mechanisms of muscle maintenance and degeneration in the context of aging and disease.
Language	English
Publishing date	2024-02-29
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.02.26.582103
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Article ; Online: Oxidative stress induced by UVA photoactivation of the tryptophan UVB photoproduct 6-formylindolo[3,2-b]carbazole (FICZ) inhibits nucleotide excision repair in human cells.

Brem, Reto / Macpherson, Peter / Guven, Melisa / Karran, Peter

Scientific reports

2017 Volume 7, Issue 1, Page(s) 4310

Abstract: Potentially mutagenic DNA lesions induced by UVB (wavelengths 280-320 nm) are important risk factors for solar ultraviolet (UV) radiation-induced skin cancer. The carcinogenicity of the more abundant UVA (320-400 nm) is less well understood but is ... ...

Abstract	Potentially mutagenic DNA lesions induced by UVB (wavelengths 280-320 nm) are important risk factors for solar ultraviolet (UV) radiation-induced skin cancer. The carcinogenicity of the more abundant UVA (320-400 nm) is less well understood but is generally regarded to reflect its interaction with cellular chromophores that act as photosensitisers. The arylhydrocarbon receptor agonist 6-formylindolo[3,2-b] carbazole (FICZ), is a UVB photoproduct of tryptophan and a powerful UVA chromophore. Combined with UVA, FICZ generates reactive oxygen species (ROS) and induces oxidative DNA damage. Here we demonstrate that ROS generated by FICZ/UVA combinations also cause extensive protein damage in HaCaT human keratinocytes. We show that FICZ/UVA-induced oxidation significantly inhibits the removal of potentially mutagenic UVB-induced DNA photolesions by nucleotide excision repair (NER). DNA repair inhibition is due to FICZ/UVA-induced oxidation damage to the NER proteome and DNA excision repair is impaired in extracts prepared from FICZ/UVA-treated cells. NER protects against skin cancer. As a likely UVB photoproduct of intracellular tryptophan, FICZ represents a de facto endogenous UVA photosensitiser in sun-exposed skin. FICZ formation may increase the risk of solar UV-induced skin cancer by promoting photochemical damage to the NER proteome and thereby preventing the removal of UVB-induced DNA lesions.
MeSH term(s)	Carbazoles/pharmacology ; DNA Damage ; DNA Repair/drug effects ; DNA Repair/radiation effects ; Humans ; Oxidation-Reduction ; Oxidative Stress/radiation effects ; Tryptophan/metabolism ; Ultraviolet Rays/adverse effects
Chemical Substances	Carbazoles ; carbazole (0P2197HHHN) ; Tryptophan (8DUH1N11BX)
Language	English
Publishing date	2017-06-27
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-017-04614-8
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Article ; Online: Deletion of Neuronal CuZnSOD Accelerates Age-Associated Muscle Mitochondria and Calcium Handling Dysfunction That Is Independent of Denervation and Precedes Sarcopenia.

Su, Yu / Claflin, Dennis R / Huang, Meixiang / Davis, Carol S / Macpherson, Peter C D / Richardson, Arlan / Van Remmen, Holly / Brooks, Susan V

International journal of molecular sciences

2021 Volume 22, Issue 19

Abstract: Skeletal muscle suffers atrophy and weakness with aging. Denervation, oxidative stress, and mitochondrial dysfunction are all proposed as contributors to age-associated muscle loss, but connections between these factors have not been established. We ... ...

Abstract	Skeletal muscle suffers atrophy and weakness with aging. Denervation, oxidative stress, and mitochondrial dysfunction are all proposed as contributors to age-associated muscle loss, but connections between these factors have not been established. We examined contractility, mitochondrial function, and intracellular calcium transients (ICTs) in muscles of mice throughout the life span to define their sequential relationships. We performed these same measures and analyzed neuromuscular junction (NMJ) morphology in mice with postnatal deletion of neuronal
MeSH term(s)	Aging ; Animals ; Calcium/metabolism ; Denervation ; Female ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondria, Muscle/metabolism ; Mitochondria, Muscle/pathology ; Muscle Contraction ; Neurons/metabolism ; Neurons/pathology ; Oxidation-Reduction ; Oxidative Stress ; Sarcopenia/etiology ; Sarcopenia/pathology ; Superoxide Dismutase-1/physiology
Chemical Substances	Sod1 protein, mouse (EC 1.15.1.1) ; Superoxide Dismutase-1 (EC 1.15.1.1) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2021-10-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms221910735
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Article ; Online: Repairing Volumetric Muscle Loss in the Ovine Peroneus Tertius Following a 6-Month Recovery.

Rodriguez, Brittany L / Novakova, Stoyna S / Vega-Soto, Emmanuel E / Nutter, Genevieve P / Macpherson, Peter C D / Larkin, Lisa M

Tissue engineering. Part A

2021 Volume 28, Issue 13-14, Page(s) 606–620

Abstract: Tissue-engineered skeletal muscle is a promising novel therapy for the treatment of volumetric muscle loss (VML). Our laboratory has developed tissue-engineered skeletal muscle units (SMUs) and engineered neural conduits (ENCs), and modularly scaled them ...

Abstract	Tissue-engineered skeletal muscle is a promising novel therapy for the treatment of volumetric muscle loss (VML). Our laboratory has developed tissue-engineered skeletal muscle units (SMUs) and engineered neural conduits (ENCs), and modularly scaled them to clinically relevant sizes for the treatment of VML in a large animal (sheep) model. In a previous study, we evaluated the effects of the SMUs and ENCs in treating a 30% VML injury in the ovine peroneus tertius muscle after a 3-month recovery period. The goal of the current study was to expand on our 3-month study and evaluate the SMUs and ENCs in restoring muscle function after a 6-month recovery period. Six months after implantation, we found that the repair groups with the SMU (VML+SMU and VML+SMU+ENC) restored muscle mass to a level that was statistically indistinguishable from the uninjured contralateral muscle. In contrast, the muscle mass in the VML-Only group was significantly less than groups repaired with an SMU. Following the 6-month recovery from VML, the maximum tetanic force was significantly lower for all VML injured groups compared with the uninjured contralateral muscle. However, we did demonstrate the ability of our ENCs to effectively regenerate nerve between the distal stump of the native nerve and the repair site in 14 of the 15 animals studied. Impact Statement Volumetric muscle loss (VML) is a clinically relevant problem for which current treatment options are lacking and for which tissue-engineered skeletal muscle presents a promising novel therapeutic option. However, the fabrication of tissues of clinically relevant sizes is necessary for advancement of the technology to the clinic. This study aimed to evaluate the efficacy of our scaled-up tissue-engineered skeletal muscle to treat VML in a large animal (sheep) model after a 6-month recovery.
MeSH term(s)	Animals ; Muscle, Skeletal/injuries ; Muscular Diseases/therapy ; Prostheses and Implants ; Sheep ; Tissue Engineering
Language	English
Publishing date	2021-12-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2420582-5
ISSN	1937-335X ; 1937-3341
ISSN (online)	1937-335X
ISSN	1937-3341
DOI	10.1089/ten.TEA.2021.0187
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Article ; Online: Transgenic expression of SOD1 specifically in neurons of Sod1 deficient mice prevents defects in muscle mitochondrial function and calcium handling.

Su, Yu / Ahn, Bumsoo / Macpherson, Peter C D / Ranjit, Rojina / Claflin, Dennis R / Van Remmen, Holly / Brooks, Susan V

Free radical biology & medicine

2021 Volume 165, Page(s) 299–311

Abstract: Aging is accompanied by loss of muscle mass and force, known as sarcopenia. Muscle atrophy, weakness, and neuromuscular junction (NMJ) degeneration reminiscent of normal muscle aging are observed early in adulthood for mice deficient in Cu, Zn-superoxide ...

Abstract	Aging is accompanied by loss of muscle mass and force, known as sarcopenia. Muscle atrophy, weakness, and neuromuscular junction (NMJ) degeneration reminiscent of normal muscle aging are observed early in adulthood for mice deficient in Cu, Zn-superoxide dismutase (SOD, Sod1
MeSH term(s)	Animals ; Calcium/metabolism ; Mice ; Mice, Transgenic ; Mitochondria ; Muscle, Skeletal/metabolism ; Neurons/metabolism ; Superoxide Dismutase/genetics ; Superoxide Dismutase/metabolism ; Superoxide Dismutase-1/genetics ; Superoxide Dismutase-1/metabolism
Chemical Substances	Sod1 protein, mouse (EC 1.15.1.1) ; Superoxide Dismutase (EC 1.15.1.1) ; Superoxide Dismutase-1 (EC 1.15.1.1) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2021-02-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2021.01.047
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Article ; Online: Removal of

Guzman, Steve D / Judge, Jennifer / Shigdar, Shahjahan M / Paul, Thomas A / Davis, Carol S / Macpherson, Peter C / Markworth, James F / Van Remmen, Holly / Richardson, Arlan / McArdle, Anne / Brooks, Susan V

Frontiers in aging

2022 Volume 2, Page(s) 821904

Abstract: Aging results in the progressive accumulation of senescent cells in tissues that display loss of proliferative capacity and acquire a senescence-associated secretory phenotype (SASP). The tumor suppressor, ... ...

Abstract	Aging results in the progressive accumulation of senescent cells in tissues that display loss of proliferative capacity and acquire a senescence-associated secretory phenotype (SASP). The tumor suppressor, p16
Language	English
Publishing date	2022-01-26
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	3076785-4
ISSN	2673-6217 ; 2673-6217
ISSN (online)	2673-6217
ISSN	2673-6217
DOI	10.3389/fragi.2021.821904
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