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Article ; Online: Butyrate Feeding Reverses CypD-Related Mitoflash Phenotypes in Mouse Myofibers

Ang Li / Xuejun Li / Jianxun Yi / Jianjie Ma / Jingsong Zhou

International Journal of Molecular Sciences, Vol 22, Iss 7412, p

2021 Volume 7412

Abstract: Mitoflashes are spontaneous transients of the biosensor mt-cpYFP. In cardiomyocytes, mitoflashes are associated with the cyclophilin D (CypD) mediated opening of mitochondrial permeability transition pore (mPTP), while in skeletal muscle they are ... ...

Abstract	Mitoflashes are spontaneous transients of the biosensor mt-cpYFP. In cardiomyocytes, mitoflashes are associated with the cyclophilin D (CypD) mediated opening of mitochondrial permeability transition pore (mPTP), while in skeletal muscle they are considered hallmarks of mitochondrial respiration burst under physiological conditions. Here, we evaluated the potential association between mitoflashes and the mPTP opening at different CypD levels and phosphorylation status by generating three CypD derived fusion constructs with a red shifted, pH stable Ca 2+ sensor jRCaMP1b. We observed perinuclear mitochondrial Ca 2+ efflux accompanying mitoflashes in CypD and CypDS42A (a phosphor-resistant mutation at Serine 42) overexpressed myofibers but not the control myofibers expressing the mitochondria-targeting sequence of CypD (CypDN30). Assisted by a newly developed analysis program, we identified shorter, more frequent mitoflash activities occurring over larger areas in CypD and CypDS42A overexpressed myofibers than the control CypDN30 myofibers. These observations provide an association between the elevated CypD expression and increased mitoflash activities in hindlimb muscles in an amyotrophic lateral sclerosis (ALS) mouse model previously observed. More importantly, feeding the mice with sodium butyrate reversed the CypD-associated mitoflash phenotypes and protected against ectopic upregulation of CypD, unveiling a novel molecular mechanism underlying butyrate mediated alleviation of ALS progression in the mouse model.
Keywords	butyrate ; mPTP ; cyclopilin D ; amyotrophic lateral sclerosis ; jRCaMP1b ; supervised inspection of Ca 2+ transients ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	333
Language	English
Publishing date	2021-07-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Mitochondrial Membrane Potential Identifies a Subpopulation of Mesenchymal Progenitor Cells to Promote Angiogenesis and Myocardial Repair

Xiuchun Li / Xiaoliang Wang / Pan He / Edward Bennett / Erin Haggard / Jianjie Ma / Chuanxi Cai

Cells, Vol 11, Iss 1713, p

2022 Volume 1713

Abstract: Identifying effective donor cells is one of obstacles that limits cell therapy for heart disease. In this study, we sorted a subpopulation of human mesenchymal progenitor cells (hMPCs) from the right atrial appendage using the low mitochondrial membrane ... ...

Abstract	Identifying effective donor cells is one of obstacles that limits cell therapy for heart disease. In this study, we sorted a subpopulation of human mesenchymal progenitor cells (hMPCs) from the right atrial appendage using the low mitochondrial membrane potential. Compared to the non-sorted cells, hMPCs hold the capacity for stemness and enrich mesenchymal stem cell markers. The hMPCs display better ability for survival, faster proliferation, less production of reactive oxygen species (ROS), and greater release of cytoprotective cytokines. The hMPCs exhibit decreased expression of senescence genes and increased expression of anti-apoptotic and antioxidant genes. Intramyocardial injection of hMPCs into the infarcted heart resulted in increased left ventricular ejection fraction and reduced cardiac remodeling and infarct size in the group of animals receiving hMPCs. Both in vitro and in vivo studies indicated hMPCs have the potential to differentiate into endothelial cells and smooth muscle cells. Immunohistochemistry staining showed that cell therapy with hMPCs enhances cardiac vascular regeneration and cardiac proliferation, and decreases cardiac cell apoptosis, which is associated with the increased secretion of cytoprotective and pro-angiogenic cytokines. Overall, we discovered a subpopulation of human mesenchymal progenitor cells via their low mitochondrial membrane potential, which might provide an alternative donor cell source for cellular therapy for ischemic heart disease.
Keywords	mitochondrial membrane potential ; mesenchymal progenitor cells ; cytokine ; angiogenesis ; myocardial infarction ; heart failure ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2022-05-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Cardiac effects and clinical applications of MG53

Weina Zhong / Dathe Z. Benissan-Messan / Jianjie Ma / Chuanxi Cai / Peter H. U. Lee

Cell & Bioscience, Vol 11, Iss 1, Pp 1-

2021 Volume 10

Abstract: Abstract Heart disease remains the leading cause of mortality globally, so further investigation is required to identify its underlying mechanisms and potential targets for treatment and prevention. Mitsugumin 53 (MG53), also known as TRIM72, is a TRIM ... ...

Abstract	Abstract Heart disease remains the leading cause of mortality globally, so further investigation is required to identify its underlying mechanisms and potential targets for treatment and prevention. Mitsugumin 53 (MG53), also known as TRIM72, is a TRIM family protein that was found to be involved in cell membrane repair and primarily found in striated muscle. Its role in skeletal muscle regeneration and myogenesis has been well documented. However, accumulating evidence suggests that MG53 has a potentially protective role in heart tissue, including in ischemia/reperfusion injury of the heart, cardiomyocyte membrane injury repair, and atrial fibrosis. This review summarizes the regulatory role of MG53 in cardiac tissues, current debates regarding MG53 in diabetes and diabetic cardiomyopathy, as well as highlights potential clinical applications of MG53 in treating cardiac pathologies.
Keywords	MG53 ; Heart disease ; Membrane repair ; Cardioprotection ; Diabetes ; Biotechnology ; TP248.13-248.65 ; Biology (General) ; QH301-705.5 ; Biochemistry ; QD415-436
Subject code	610
Language	English
Publishing date	2021-06-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Calcium signaling

Xuehong Xu / Steven P. Balk / William B. Isaacs / Jianjie Ma

Cell & Bioscience, Vol 8, Iss 1, Pp 1-

an underlying link between cardiac disease and carcinogenesis

2018 Volume 2

Keywords	Biotechnology ; TP248.13-248.65 ; Biology (General) ; QH301-705.5 ; Biochemistry ; QD415-436
Language	English
Publishing date	2018-06-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Efficient precise in vivo base editing in adult dystrophic mice

Li Xu / Chen Zhang / Haiwen Li / Peipei Wang / Yandi Gao / Nahush A. Mokadam / Jianjie Ma / W. David Arnold / Renzhi Han

Nature Communications, Vol 12, Iss 1, Pp 1-

2021 Volume 14

Abstract: Base editing is one approach used to correct mutations causing cause Duchenne muscular dystrophy (DMD), but limitations are in the requirement for a specific PAM motif and the large size beyond the packaging capacity of adeno-associated virus (AAV). Here, ...

Abstract	Base editing is one approach used to correct mutations causing cause Duchenne muscular dystrophy (DMD), but limitations are in the requirement for a specific PAM motif and the large size beyond the packaging capacity of adeno-associated virus (AAV). Here, the authors modify the NG-targeting adenine base editor to recognize a broader PAM, devise an intein split strategy to package the otherwise oversized adenine base editor into AAV, and show it efficiently restores dystrophin expression in muscle and heart when systemically injected in a mouse model of DMD
Keywords	Science ; Q
Language	English
Publishing date	2021-06-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: MG53, A Tissue Repair Protein with Broad Applications in Regenerative Medicine

Zhongguang Li / Liyang Wang / Huimin Yue / Bryan A. Whitson / Erin Haggard / Xuehong Xu / Jianjie Ma

Cells, Vol 10, Iss 122, p

2021 Volume 122

Abstract: Under natural conditions, injured cells can be repaired rapidly through inherent biological processes. However, in the case of diabetes, cardiovascular disease, muscular dystrophy, and other degenerative conditions, the natural repair process is impaired. ...

Abstract	Under natural conditions, injured cells can be repaired rapidly through inherent biological processes. However, in the case of diabetes, cardiovascular disease, muscular dystrophy, and other degenerative conditions, the natural repair process is impaired. Repair of injury to the cell membrane is an important aspect of physiology. Inadequate membrane repair function is implicated in the pathophysiology of many human disorders. Recent studies show that Mitsugumin 53 (MG53), a TRIM family protein, plays a key role in repairing cell membrane damage and facilitating tissue regeneration. Clarifying the role of MG53 and its molecular mechanism are important for the application of MG53 in regenerative medicine. In this review, we analyze current research dissecting MG53′s function in cell membrane repair and tissue regeneration, and highlight the development of recombinant human MG53 protein as a potential therapeutic agent to repair multiple-organ injuries.
Keywords	TRIM protein ; cell membrane repair ; muscular dystrophy ; myocardial infarction ; acute kidney injury ; acute lung injury ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2021-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Physical exercise

Xinjuan Lei / Yajun Wu / MengMeng Xu / Odell D. Jones / Jianjie Ma / Xuehong Xu

Cell & Bioscience, Vol 9, Iss 1, Pp 1-

bulking up neurogenesis in human adults

2019 Volume 4

Abstract: Abstract Whether neurogenesis occurs in the adult human brain has been a long-debated topic fueled by conflicting data both for and against neurogenesis in the mature brain. Recent reports from two independent teams may have indubitably proven that adult, ...

Abstract	Abstract Whether neurogenesis occurs in the adult human brain has been a long-debated topic fueled by conflicting data both for and against neurogenesis in the mature brain. Recent reports from two independent teams may have indubitably proven that adult, hippocampal neurogenesis persists throughout the human lifespan. Llorens-Martín et al. found that thousands of immature, neurogenesis related, doublecortin-positive (DCX+) labelled neurons can be detected in the human dentate gyrus (DG) up to the eighth decade of life. While the presence of these DCX+ neurons decrease with age, they are significantly decrease in patient with Alzheimer’s disease. Another group have also found mammalian embryonic Hopx+ precursors to persist beyond the early development stage as quiescent Hopx+ radial glial-like neural progenitors during early postnatal period, then as Hopx+ adult dentate neural progenitors. Together, the findings from these two groups suggest that unlike the previously thought, neurogenesis and neuroplasticity can occur well into adulthood in some capacity, at least in the hippocampus. These recent findings that neurogenesis can occur beyond development have brought into questions whether physical exercise can be shown to promote neurogenesis and brain health, as it has been shown to promote the function of other organ systems. Some data has already shown physical exercise to induce adult hippocampal neurogenesis (AHN) as demonstrated by restoration of cognitive functions, improvement of synaptic plasticity, and enhancement of angiogenesis. A large-scale meta-analysis has also demonstrated that 45–60 min of moderate-intensity physical exercise to dramatically improve cognitive functions in human subjects over the age of 50. Given these convergent developments in our understanding of neurogenesis and exercise induced improvement in cognitive function, we speculate that hippocampal neurogenesis can be promoted by physical exercise and discuss the current molecular evidence supporting the likely molecular pathways ...
Keywords	Neurogenesis ; Adult ; Physical exercise ; Cognitive function ; Biotechnology ; TP248.13-248.65 ; Biology (General) ; QH301-705.5 ; Biochemistry ; QD415-436
Subject code	120
Language	English
Publishing date	2019-09-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Exercise-induced myokine FNDC5/irisin functions in cardiovascular protection and intracerebral retrieval of synaptic plasticity

Xin Zhou / MengMeng Xu / Joseph L. Bryant / Jianjie Ma / Xuehong Xu

Cell & Bioscience, Vol 9, Iss 1, Pp 1-

2019 Volume 4

Abstract: Abstract Physical exercise is well known to benefit human health at every age. However, the exact mechanism through which physical exercise improves health remains unknown. Recent studies into exercise-induced myokine FNDC5/irisin, a newly discovered ... ...

Abstract	Abstract Physical exercise is well known to benefit human health at every age. However, the exact mechanism through which physical exercise improves health remains unknown. Recent studies into exercise-induced myokine FNDC5/irisin, a newly discovered hormone, have begun to shed light on this mystery. Exercise-induced myokine FNDC5/irisin have been shown to be protective against cardiovascular damage post ischemic event, improve function in the neurons of Alzheimer’s disease patients, and have been implicated in macrophage and adipocyte regulation. Elegantly designed experiments have shown FNDC5/irisin to promote Nkx2.5+ cardiac progenitor cell dependent cardiac regeneration, neovascularization, and reduce cardiac fibrosis. It has also been shown to improve macrophage function, which may protect against injuries to the cardiac conduction system. Similarly, FNDC5/irisin knockout mice have been shown to have reduced memory performance, while peripheral overexpression of FNDC5/irisin has been shown to improve memory impairment in a murine Alzheimer’s disease model. Finally, FNDC5/irisin has been linked to regulation of osteocytes and adipocytes by signaling through the cytoplasmic membrane integrated protein aV/b5 integrin, the first known receptor for this newly discovered hormone. Although these recent discoveries have cemented the importance of FNDC5/irisin, many details regarding how FNDC5/irisin fits into the physiology of exercise benefits remain unknown and are deserving of future inquiry.
Keywords	Biotechnology ; TP248.13-248.65 ; Biology (General) ; QH301-705.5 ; Biochemistry ; QD415-436
Subject code	796
Language	English
Publishing date	2019-04-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: MG53 preserves mitochondrial integrity of cardiomyocytes during ischemia reperfusion-induced oxidative stress

Kristyn Gumpper-Fedus / Ki Ho Park / Hanley Ma / Xinyu Zhou / Zehua Bian / Karthikeyan Krishnamurthy / Matthew Sermersheim / Jingsong Zhou / Tao Tan / Lei Li / Jianxun Liu / Pei-Hui Lin / Hua Zhu / Jianjie Ma

Redox Biology, Vol 54, Iss , Pp 102357- (2022)

2022

Abstract: Ischemic injury to the heart induces mitochondrial dysfunction due to increasing oxidative stress. MG53, also known as TRIM72, is highly expressed in striated muscle, is secreted as a myokine after exercise, and is essential for repairing damaged plasma ... ...

Abstract	Ischemic injury to the heart induces mitochondrial dysfunction due to increasing oxidative stress. MG53, also known as TRIM72, is highly expressed in striated muscle, is secreted as a myokine after exercise, and is essential for repairing damaged plasma membrane of many tissues by interacting with the membrane lipid phosphatidylserine (PS). We hypothesized MG53 could preserve mitochondrial integrity after an ischemic event by binding to the mitochondrial-specific lipid, cardiolipin (CL), for mitochondria protection to prevent mitophagy. Fluorescent imaging and Western blotting experiments showed recombinant human MG53 (rhMG53) translocated to the mitochondria after ischemic injury in vivo and in vitro. Fluorescent imaging indicated rhMG53 treatment reduced superoxide generation in ex vivo and in vitro models. Lipid-binding assay indicated MG53 binds to CL. Transfecting cardiomyocytes with the mitochondria-targeted mt-mKeima showed inhibition of mitophagy after MG53 treatment. Overall, we show that rhMG53 treatment may preserve cardiac function by preserving mitochondria in cardiomyocytes. These findings suggest MG53's interactions with mitochondria could be an attractive avenue for developing MG53 as a targeted protein therapy for cardioprotection.
Keywords	Cardioprotection ; Mitophagy ; Cell membrane repair ; TRIM72 ; Myocardial infarction ; Cardiolipin ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2022-08-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Sustained delivery of rhMG53 promotes diabetic wound healing and hair follicle development

Hong Niu / Haichang Li / Ya Guan / Xin Zhou / Zhongguang Li / Serana Li Zhao / Peng Chen / Tao Tan / Hua Zhu / Valerie Bergdall / Xuehong Xu / Jianjie Ma / Jianjun Guan

Bioactive Materials, Vol 18, Iss , Pp 104-

2022 Volume 115

Abstract: MG53 is an essential component of the cell membrane repair machinery, participating in the healing of dermal wounds. Here we develop a novel delivery system using recombinant human MG53 (rhMG53) protein and a reactive oxygen species (ROS)-scavenging gel ... ...

Abstract	MG53 is an essential component of the cell membrane repair machinery, participating in the healing of dermal wounds. Here we develop a novel delivery system using recombinant human MG53 (rhMG53) protein and a reactive oxygen species (ROS)-scavenging gel to treat diabetic wounds. Mice with ablation of MG53 display defective hair follicle structure, and topical application of rhMG53 can promote hair growth in the mg53−/− mice. Cell lineage tracing studies reveal a physiological function of MG53 in modulating the proliferation of hair follicle stem cells (HFSCs). We find that rhMG53 protects HFSCs from oxidative stress-induced apoptosis and stimulates differentiation of HSFCs into keratinocytes. The cytoprotective function of MG53 is mediated by STATs and MAPK signaling in HFSCs. The thermosensitive ROS-scavenging gel encapsulated with rhMG53 allows for sustained release of rhMG53 and promotes healing of chronic cutaneous wounds and hair follicle development in the db/db mice. These findings support the potential therapeutic value of using rhMG53 in combination with ROS-scavenging gel to treat diabetic wounds.
Keywords	Diabetic wound healing ; hair follicle stem cell ; MG53 ; ROS-Scavenging hydrogel ; Controlled drug delivery ; Materials of engineering and construction. Mechanics of materials ; TA401-492 ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2022-12-01T00:00:00Z
Publisher	KeAi Communications Co., Ltd.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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