Jianjie Ma

ORCID: 0000-0003-3865-6112
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About
Contact & Profiles
Research Areas
  • Muscle Physiology and Disorders
  • Mitochondrial Function and Pathology
  • Amyotrophic Lateral Sclerosis Research
  • Ion channel regulation and function
  • Adipose Tissue and Metabolism
  • Cardiac Ischemia and Reperfusion
  • interferon and immune responses
  • Calcium signaling and nucleotide metabolism
  • Ion Channels and Receptors
  • Autophagy in Disease and Therapy
  • Cystic Fibrosis Research Advances
  • Neonatal Respiratory Health Research
  • RNA Interference and Gene Delivery
  • Endoplasmic Reticulum Stress and Disease
  • Tissue Engineering and Regenerative Medicine
  • Cell death mechanisms and regulation
  • Cardiomyopathy and Myosin Studies
  • Advanced biosensing and bioanalysis techniques
  • Neurobiology and Insect Physiology Research
  • Signaling Pathways in Disease
  • Immune Response and Inflammation
  • Cellular transport and secretion
  • Cellular Mechanics and Interactions
  • Wound Healing and Treatments
  • Cardiac electrophysiology and arrhythmias

University of Virginia
2022-2025

Lung Institute
2014-2025

The Ohio State University
2015-2025

National Yang Ming Chiao Tung University
2024-2025

The Ohio State University Wexner Medical Center
2015-2024

The University of Texas at Arlington
2019-2024

Temple University
2023-2024

Indian Institute of Science Bangalore
2023-2024

Fred Hutch Cancer Center
2024

TRIM edicine (United States)
2012-2021

Elevated lipogenesis regulated by sterol regulatory element-binding protein-1 (SREBP-1), a transcription factor playing central role in lipid metabolism, is novel characteristic of glioblastoma (GBM). The aim this study was to identify effective approaches suppress GBM growth inhibition SREBP-1. As SREBP activation negatively endoplasmic reticulum (ER) cholesterol, we sought determine whether suppression O-acyltransferase (SOAT), key enzyme converting ER cholesterol esters (CE) store...

10.1158/1078-0432.ccr-15-2973 article EN Clinical Cancer Research 2016-06-09

Duchenne muscular dystrophy (DMD) is a degenerative muscle disease caused by genetic mutations that lead to the disruption of dystrophin in fibers. There no curative treatment for this devastating disease. Clustered regularly interspaced short palindromic repeat/Cas9 (CRISPR/Cas9) has emerged as powerful tool manipulation and potential therapy. Here we demonstrate CRIPSR-mediated genome editing efficiently excised 23-kb genomic region on X-chromosome covering mutant exon 23 mouse model DMD,...

10.1038/mt.2015.192 article EN cc-by-nc-nd Molecular Therapy 2015-10-09

Cytochrome c is released from mitochondria into the cytosol in cells undergoing apoptosis. The temporal relationship between cytochrome release and loss of mitochondrial membrane potential was monitored by laser-scanning confocal microscopy single living pheochromocytoma-6 apoptosis induced staurosporine. Mitochondrial tetramethylrhodamine methyl ester decreased abruptly individual 2 to 7 h after treatment with Depolarization accompanied cytochromec documented transfected green fluorescent...

10.1074/jbc.274.9.5654 article EN cc-by Journal of Biological Chemistry 1999-02-01

Abstract The up-regulation of phase II detoxifying and stress-responsive genes is believed to play an important role in cancer prevention, many natural compounds have been shown be potent inducers these genes. Previous studies showed that the antioxidant responsive element (ARE), found genes, can bound by transcription factor Nrf2, activation chemopreventive oxidative stress. In present study, we investigated roles extracellular signal-regulated kinase (ERK) c-Jun-NH2-kinase (JNK) regulation...

10.1158/1535-7163.mct-05-0497 article EN Molecular Cancer Therapeutics 2006-08-01

Abstract The present study was designed to investigate the effects of two main constituents green tea, (−)-epigallocatechin-3-gallate (EGCG) and caffeine, on intestinal tumorigenesis in Apcmin/+ mice, a recognized mouse model for human cancer, elucidate possible mechanisms involved inhibitory action active constituent. We found that p.o. administration EGCG at doses 0.08% or 0.16% drinking fluid significantly decreased small tumor formation by 37% 47%, respectively, whereas caffeine dose...

10.1158/0008-5472.can-05-1949 article EN Cancer Research 2005-11-15

Unrepaired cardiomyocyte membrane injury causes irreplaceable cell loss, leading to myocardial fibrosis and eventually heart failure. However, the cellular molecular mechanisms of cardiac repair are largely unknown. MG53, a newly identified striated muscle-specific protein, is involved in skeletal muscle repair. But role MG53 has not been determined.We sought investigate whether mediates cardiomyocytes and, if so, mechanism underlying MG53-mediated cardiomyocytes. Moreover, we determined...

10.1161/circresaha.109.215822 article EN Circulation Research 2010-05-14

Quantum confined materials have been extensively studied for photoluminescent applications. Due to intrinsic limitations of low biocompatibility and challenging modulation, the utilization conventional inorganic quantum in bio-imaging bio-machine interface faces critical restrictions. Here, we present aromatic cyclo-dipeptides that dimerize into dots, which serve as building blocks further self-assemble supramolecular structures with diverse morphologies photoluminescence properties....

10.1038/s41467-018-05568-9 article EN cc-by Nature Communications 2018-08-07

Biopolymeric hydrogels have drawn increasing research interest in biomaterials due to their tunable physical and chemical properties for both creating bioactive cellular microenvironment serving as sustainable therapeutic reagents. Inspired by a naturally occurring hydrogel secreted from the carnivorous Sundew plant trapping insects, here we developed bioinspired deliver mitsugumin 53 (MG53), an important protein cell membrane repair, chronic wound healing. Both compositions...

10.1021/acsami.7b04428 article EN ACS Applied Materials & Interfaces 2017-06-22

Rationale: Duchenne muscular dystrophy is a severe inherited form of caused by mutations in the reading frame dystrophin gene disrupting its protein expression. Dystrophic cardiomyopathy leading cause death patients, and currently no effective treatment exists to halt progression. Recent advancement genome editing technologies offers promising therapeutic approach restoring However, impact this on cardiac function has yet be evaluated. Therefore, we assessed efficacy CRISPR (clustered...

10.1161/circresaha.117.310996 article EN Circulation Research 2017-08-09

Mitochondria-targeting peptides have garnered immense interest as potential chemotherapeutics in recent years. However, there is a clear need to develop strategies overcome the critical limitations of peptides, such poor solubility and lack target specificity, which impede their clinical applications. To this end, we report magnetic core–shell nanoparticle (MCNP)-mediated delivery mitochondria-targeting pro-apoptotic amphipathic tail-anchoring peptide (ATAP) malignant brain metastatic breast...

10.1021/nn503431x article EN publisher-specific-oa ACS Nano 2014-08-18

Oxygen deficiency after myocardial infarction (MI) leads to massive cardiac cell death. Protection of cells and promotion repair are key therapeutic goals. These goals may be achieved by re-introducing oxygen into the infarcted area. Yet current systemic delivery approaches cannot efficiently diffuse area that has extremely low blood flow. In this work, we developed a new system can delivered specifically tissue, continuously release protect cells. The was based on thermosensitive,...

10.1038/s41598-018-19906-w article EN cc-by Scientific Reports 2018-01-16

Recombinant MG53 translocates to sites of injury in the proximal tubule kidney and protects mice from acute induced by ischemia or drugs.

10.1126/scitranslmed.3010755 article EN Science Translational Medicine 2015-03-18

Abstract: Irisin, a muscle-origin protein derived from the extracellular domain of fibronectin domain-containing 5 (FNDC5), has been shown to modulate mitochondria welfare through paracrine action. Here, we test hypothesis that irisin contributes cardioprotection after myocardial infarction by preserving mitochondrial function in cardiomyocytes. Animal model studies show intravenous administration exogenous produces dose-dependent protection against ischemia/reperfusion (I/R)-induced injury...

10.1097/fjc.0000000000000608 article EN cc-by-nc-nd Journal of Cardiovascular Pharmacology 2018-07-04

Abstract Recent advances in base editing have created an exciting opportunity to precisely correct disease-causing mutations. However, the large size of editors and their inherited off-target activities pose challenges for vivo editing. Moreover, requirement a protospacer adjacent motif (PAM) nearby mutation site further limits targeting feasibility. Here we modify NG-targeting adenine editor (iABE-NGA) overcome these demonstrate high efficiency edit Duchenne muscular dystrophy (DMD) adult...

10.1038/s41467-021-23996-y article EN cc-by Nature Communications 2021-06-17

Ischemic injury to the heart induces mitochondrial dysfunction due increasing oxidative stress. MG53, also known as TRIM72, is highly expressed in striated muscle, secreted a myokine after exercise, and essential for repairing damaged plasma membrane of many tissues by interacting with lipid phosphatidylserine (PS). We hypothesized MG53 could preserve integrity an ischemic event binding mitochondrial-specific lipid, cardiolipin (CL), mitochondria protection prevent mitophagy. Fluorescent...

10.1016/j.redox.2022.102357 article EN cc-by-nc-nd Redox Biology 2022-06-02
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