Joseph D. Gardinier

ORCID: 0000-0002-8651-8913
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About
Contact & Profiles
Research Areas
  • Bone health and osteoporosis research
  • Bone health and treatments
  • Vitamin D Research Studies
  • Bone Metabolism and Diseases
  • Muscle activation and electromyography studies
  • Advanced Vision and Imaging
  • Gut microbiota and health
  • Adenosine and Purinergic Signaling
  • Advanced Optical Sensing Technologies
  • NF-κB Signaling Pathways
  • Fibroblast Growth Factor Research
  • Diet and metabolism studies
  • Protease and Inhibitor Mechanisms
  • Bone Tissue Engineering Materials
  • Stroke Rehabilitation and Recovery
  • Clostridium difficile and Clostridium perfringens research
  • Histone Deacetylase Inhibitors Research
  • Adipose Tissue and Metabolism
  • Exercise and Physiological Responses
  • Veterinary Equine Medical Research
  • Cardiovascular Function and Risk Factors
  • Cerebral Palsy and Movement Disorders
  • Microscopic Colitis
  • Cellular Mechanics and Interactions
  • Endodontics and Root Canal Treatments

Michigan State University
2024

Henry Ford Health System
2018-2024

Henry Ford Health + Michigan State University Health Sciences
2024

Woodward (United States)
2023

Henry Ford Hospital
2016-2022

University of Delaware
2005-2021

Biomechanics Institute of Valencia
2020

University of Michigan
2013-2018

Laboratoire de Physique des 2 Infinis Irène Joliot-Curie
2005

ABSTRACT Glucocorticoids (GCs) are potent immune-modulating drugs with significant side effects, including glucocorticoid-induced osteoporosis (GIO). GCs directly induce osteoblast and osteocyte apoptosis but also alter intestinal microbiota composition. Although the gut is known to contribute regulation of bone density, its role in GIO has never been examined. To test this, male C57/Bl6J mice were treated for 8 weeks GC (prednisolone, GC-Tx) presence or absence broad-spectrum antibiotic...

10.1002/jbmr.3947 article EN Journal of Bone and Mineral Research 2019-12-30

Antibiotic treatment, commonly prescribed for bacterial infections, depletes and subsequently causes long-term alterations in intestinal microbiota composition. Knowing the importance of microbiome regulation bone density, we investigated effect postantibiotic treatment on gut health. Intestinal repopulation at 4-weeks resulted an increase Firmicutes:Bacteroidetes ratio, increased permeability, notably reduced femoral trabecular volume (approximately 30%, p < 0.01). Treatment with a mucus...

10.1002/jbmr.3635 article EN Journal of Bone and Mineral Research 2019-01-28

Improving the structural integrity of bone reduces fracture risk and development osteoporosis later in life. Exercise can increase mechanical properties bone, this is often attributed to dynamic loading created during exercise. However, systemic parathyroid hormone (PTH) levels exercise gives reason hypothesize that PTH signaling also regulates adaptation response Therefore, first aim study was establish impact has on by inhibiting with PTH(7-34); second determine whether increasing...

10.1002/jbmr.2432 article EN Journal of Bone and Mineral Research 2014-12-22

Exercise is a key determinate of fracture risk and provides clinical means to promote bone formation. However, the efficacy exercise increase mass declines with age. The purpose this study was identify age-related differences in anabolic response at cellular tissue level. To end, young (8-weeks age) adult (36-weeks male mice were subjected moderate regimen running on treadmill. As result, had significant effect PTHrP SOST gene expression during first week that dependent upon In particular,...

10.1016/j.bonr.2018.01.003 article EN cc-by Bone Reports 2018-01-12

Mechanical stimulation of osteoblasts activates many cellular mechanisms including the release ATP. Binding ATP to purinergic receptors is key load-induced osteogenesis. Osteoblasts also respond fluid shear stress (FSS) with increased actin fiber formation (ASFF) that we postulate in response activation P2Y2 receptor (P2Y2R). Furthermore, predict ASFF increases cell stiffness and reduces sensitivity further mechanical stimulation. We found small interfering RNA (siRNA) suppression P2Y2R...

10.1152/ajpcell.00254.2013 article EN AJP Cell Physiology 2014-04-03

E487K point mutation of aldehyde dehydrogenase (ALDH) 2 (ALDH2*2) in East Asians intrinsically lowers ALDH2 activity. ALDH2*2 is associated with diabetic cardiomyopathy. Diabetic patients exhibit heart failure preserved ejection fraction (HFpEF) i.e. while the systolic function them, they may diastolic dysfunction, implying a jeopardized myocardial health. Currently, it challenging to detect cardiac functional deterioration mice. Stress echocardiography (echo) clinical set-up procedure used...

10.1371/journal.pone.0195796 article EN cc-by PLoS ONE 2018-04-20

Exercise and physical activity are critical to maintain bone mass strength throughout life. Both exercise subject a unique combination of stimuli in the forms dynamic loading systemic increase parathyroid hormone (PTH). Although is considered be primary osteogenic stimuli, influence increasing PTH levels remains unclear. We hypothesize that activation PTH/PTH-related peptide type 1 receptor (PPR) along osteoblast lineage facilitates formation improved mechanical properties response exercise....

10.1371/journal.pone.0211076 article EN cc-by PLoS ONE 2019-01-25

ABSTRACT Glucocorticoids (GCs) are commonly used anti‐inflammatory medications with significant side effects, including glucocorticoid‐induced osteoporosis (GIO). We have previously demonstrated that chronic subcutaneous GC treatment in mice leads to gut barrier dysfunction and trabecular bone loss. further showed treating probiotics or enhancers improves function prevents GIO. The overall goal of this study was test if could prevent GC‐induced loss a clinically relevant oral‐GC model...

10.1002/jbm4.10805 article EN cc-by JBMR Plus 2023-08-13

Osteocytes’ response to dynamic loading plays a crucial role in regulating the bone mass but quickly becomes saturated such that downstream induction of formation plateaus. The underlying mechanisms downregulate osteocytes’ sensitivity and overall remain unknown. In other cell types, purinergic signaling through P2Y2 receptor has potential by modifying stiffness actin polymerization cytoskeleton organization. Herein, we examined activation mechanotransduction using knockout line alongside...

10.1083/jcb.202403005 article EN The Journal of Cell Biology 2024-08-30

The breakdown of the polymeric component contemporary composite dental restorative materials compromises their longevity, while leachable compounds from these have cellular consequences. Thus, a new generation needed to be designed longer service life and ensure that any are not harmful appropriate cell lines. To accomplish this, we developed concurrent thiol-ene-based polymerization allyl sulfide-based addition-fragmentation chain transfer chemistries afford cross-linked resins demonstrate...

10.1177/0022034518795673 article EN Journal of Dental Research 2018-09-06

Age-related bone loss is attributed to the accumulation of senescent cells and their increasing production inflammatory cytokines as part senescence-associated secretory phenotype (SASP). In otherwise healthy individuals, osteocytes play a key role in maintaining mass through primary function responding skeletal loading. Given that osteocytes' response loading known steadily decline with age, we hypothesized presence SASP inhibit To test this hypothesis, developed two vitro models...

10.1002/jcp.30690 article EN Journal of Cellular Physiology 2022-02-01

ABSTRACT As the aging population continues to grow, incidence of osteoporotic fractures increases and is compounded by our lack therapeutic strategies that increase bone formation. Although exercise physical activity play a key role in maintaining mass throughout lives, loads exertion required elicit an anabolic response becomes exceedingly difficult achieve with age. Based on previous work, P2Y 2 receptor offers unique target increasing modifying mechanotransduction. Others have also shown...

10.1111/acel.14464 article EN cc-by Aging Cell 2024-12-31
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