A5060104599- Nuclear Structure and Function
- Telomeres, Telomerase, and Senescence
- Muscle Physiology and Disorders
- Mesenchymal stem cell research
- Antioxidant Activity and Oxidative Stress
- interferon and immune responses
- Natural product bioactivities and synthesis
- RNA Research and Splicing
- Wound Healing and Treatments
- Retinoids in leukemia and cellular processes
- Trace Elements in Health
- Extracellular vesicles in disease
- Bone Metabolism and Diseases
- Tendon Structure and Treatment
- Autophagy in Disease and Therapy
- Heart Rate Variability and Autonomic Control
- Environmental DNA in Biodiversity Studies
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Redox biology and oxidative stress
- Clusterin in disease pathology
- Orthopaedic implants and arthroplasty
- Cellular Mechanics and Interactions
- Musculoskeletal synovial abnormalities and treatments
- Osteoarthritis Treatment and Mechanisms
- Morinda citrifolia extract uses
Steadman Philippon Research Institute
2019-2025
Università Campus Bio-Medico
2021
Colorado State University
2021
OASI Bioresearch Foundation
2021
Steadman Clinic
2021
The University of Texas Health Science Center at Houston
2019
The University of Texas Health Science Center at San Antonio
2013-2017
The University of Texas at Arlington
2013-2016
Synaptic loss and neuron death are the underlying cause of neurodegenerative diseases such as Alzheimer's disease (AD); however, modalities cell in those remain unclear. Ferroptosis, a newly identified oxidative mechanism triggered by massive lipid peroxidation, is implicated degeneration neurons populations spinal motor midbrain neurons. Here, we investigated whether forebrain regions (cerebral cortex hippocampus) that severely afflicted AD patients might be vulnerable to ferroptosis. To...
Abstract Hutchinson–Gilford progeria syndrome (HGPS) is caused by the accumulation of mutant prelamin A (progerin) in nuclear lamina, resulting increased stiffness and abnormal architecture. Nuclear mechanics are tightly coupled to cytoskeletal via lamin A/C. However, role cytoskeletal/nuclear mechanical properties mediating cellular senescence relationship between stiffness, abnormalities, senescent phenotypes remain largely unknown. Here, using muscle‐derived mesenchymal stromal/stem cells...
Aging leads to several geriatric conditions including osteoporosis (OP) and associated frailty syndrome. Treatments for these are limited none target fundamental drivers of pathology, thus identifying strategies delay progressive loss tissue homeostasis functional reserve will significantly improve quality life in elderly individuals. A property aging is the accumulation senescent cells. Senescence a cell state defined by proliferative capacity, resistance apoptosis, release proinflammatory...
Abstract Mesenchymal stem cells (MSCs) have long been viewed as a promising therapeutic for musculoskeletal repair. However, regulatory concerns including tumorgenicity, inconsistencies in preparation techniques, donor-to-donor variability, and the accumulation of senescence during culture expansion hindered clinical application MSCs. Senescence is driving mechanism MSC dysfunction with advancing age. Often characterized by increased reactive oxygen species, senescence-associated...
Abstract Chronic conditions associated with aging have proven difficult to prevent or treat. Senescence is a cell fate defined by loss of proliferative capacity and the development pro‐inflammatory senescence‐associated secretory phenotype comprised cytokines/chemokines, proteases, other factors that promotes age‐related diseases. Specifically, an increase in senescent peripheral blood mononuclear cells (PBMCs), including T cells, like frailty, rheumatoid arthritis, bone loss. However, it...
Abstract The mechanism regulating cellular senescence of postmitotic muscle cells is still unknown. cGAS-STING innate immune signaling was found to mediate in various types cells, including neuron which however has not been explored cells. Here by studying the myofibers from Zmpste24 −/− progeria aged mice [an established model for Hutchinson-Gilford syndrome (HGPS)], we observed senescence-associated phenotypes myofibers, coupled with increased oxidative damage mitochondrial DNA (mtDNA) and...
It has long been observed that environmental conditions play crucial roles in modulating immunity and disease plants animals. For instance, many bacterial plant outbreaks occur after periods of high humidity rain. A critical step infection is entry into the interior through wounds natural openings, such as stomata, which are adjustable microscopic pores epidermal tissue. Several studies have shown stomatal closure an integral part immune response to reduce pathogen invasion. In this study,...
The aging of the immune system, or immunosenescence, was recently verified to have a causal role in driving solid organs, while senolytic elimination senescent cells found effectively delay systemic aging. Our recent study also showed that severely dystrophic muscles develop senescence-like phenotypes, including increased expression senescence-associated secretory phenotype (SASP) factors and senescence markers. Here we further investigated whether specific clearance muscle may improve...
Aging-related loss of adult stem cell function contributes to impaired tissue regeneration. Mice deficient in zinc metalloproteinase STE24 (Zmpste24-/-) exhibit premature age-related musculoskeletal pathologies similar those observed children with Hutchinson-Gilford progeria syndrome (HGPS). We have reported that muscle-derived stem/progenitor cells (MDSPCs) isolated from Zmpste24-/- mice are defective their proliferation and differentiation capabilities culture during The mechanistic target...
Abstract Background Fibro‐adipogenic progenitors (FAPs) in the muscles have been found to interact closely with muscle progenitor/stem cells (MPCs) and facilitate regeneration at normal conditions. However, it is not clear how FAPs may MPCs aged muscles. Senolytics demonstrated selectively eliminate senescent generate therapeutic benefits on ageing multiple age‐related disease models. Methods By studying primary of age matched WT mice Zmpste24 −/− (Z24 ) mice, an accelerated model for...
Mesenchymal stem cells (MSCs) have been proven to promote tissue repair. However, concerns related their clinical application and regulatory hurdles remain. Recent data has demonstrated the proregenerative secretome of MSCs can result in similar effects absence themselves. Within secretome, exosomes emerged as a promising regenerative component. Exosomes, which are nanosized lipid vesicles secreted by cells, encapsulate micro-RNA (miRNA), RNA, proteins that drive potential with cell specific...
Nuclear decoupling and softening are the main cellular mechanisms to resist mechanical stress-induced nuclear/DNA damage, however, its molecular remain much unknown. Our recent study of Hutchinson-Gilford progeria syndrome (HGPS) disease revealed role nuclear membrane protein Sun2 in mediating damages senescence cells. However, potential damage correlation with is still not clear. By applying cyclic stretch mesenchymal stromal cells (MSCs) WT Zmpset24-/- mice (Z24-/-, a model for HGPS), we...
This case report examines the impact of mild hyperbaric oxygen therapy (mHBOT) on cognitive function and symptom relief in a 35-year-old male presenting with concussive symptoms (CS) following motor vehicle accident (MVA). The patient underwent 10 mHBOT sessions over five weeks (40 minutes per session at 1.5 ATA 32% oxygen). Post-treatment assessments revealed significant improvements, including an increase P300 voltage from 4.2 µV to 9.2 µV, aligning normative range 8 - 21 µV....
Bone marrow-derived mesenchymal stem cells (BM-MSCs) are well established for their osteogenic potential but prone to senescence with aging or in vitro expansion. Drug treatments that reduce cellular may enhance the regenerative capacity of BM-MSCs. This study investigates effects losartan and fisetin, both separately combination, on osteogenesis. Human BM-MSCs were exposed low high concentrations each drug 24 h. Our findings showed high-dose exhibited cytotoxicity, focusing subsequent...
Dietary supplementation with ursolic acid (UA) prevents monocyte dysfunction in diabetic mice and protects against atherosclerosis loss of renal function. The goal this study was to determine the molecular mechanism by which UA induced metabolic stress.Metabolic stress sensitizes or "primes" human THP-1 monocytes murine peritoneal macrophages chemoattractant MCP-1, converting these cells into a hyper-chemotactic phenotype. protected priming prevented their hyper-reactivity MCP-1. blocked...
Duchenne Muscular Dystrophy (DMD) patients often suffer from both muscle wasting and osteoporosis. Our previous studies have revealed reduced regeneration potential in skeletal bone, concomitant with ectopic calcification of soft tissues double knockout (dKO, dystrophin-/-; utrophin-/-) mice, a severe murine model for DMD. We found significant involvement RhoA/ROCK (Rho-Associated Protein Kinase) signaling mediating muscles dKO mice. However, the cellular identity these RhoA+ cells, role...