Subhashis Pal

Dr. Subhashis Pal

Eris Lifesciences, Ahmedabad, India
orcid

Research Focus & Metrics

Academic Career Length

13Years (2014-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

View All Publications
3 March 2020 in Journal of Clinical Investigation
Verified
Journal Article
Open access
PDF file
JLJau-Yi Li
Jau-Yi Li
MYMingcan Yu
Mingcan Yu
Subhashis PalSubhashis Pal
Subhashis Pal
ATAbdul Malik Tyagi
Abdul Malik Tyagi
HDHamid Dar
Hamid Dar
RPRoberto Pacifici
Roberto Pacifici
Parathyroid hormone (PTH) is a critical regulator of skeletal development that promotes both bone formation and bone resorption. Using microbiota depletion by wide-spectrum antibiotics and germ-free (GF) female mice, we showed that the microbiota was required for PTH to stimulate bone formation and increase bone mass. Microbiota depletion lowered butyrate levels, a metabolite responsible for gut-bone communication, while reestablishment of physiologic levels of butyrate restored PTH-induced anabolism. The permissive activity of butyrate was mediated by GPR43 signaling in dendritic cells and by GPR43-independent signaling in T cells. Butyrate was required for PTH to increase the number of bone marrow (BM) regulatory T cells (Tregs). Tregs stimulated production of the osteogenic Wnt ligand Wnt10b by BM CD8+ T cells, which activated Wnt-dependent bone formation. Together, these data highlight the role that butyrate produced by gut luminal microbiota plays in triggering regulatory pathways, which are critical for the anabolic action of PTH in bone.

15 February 2021 in Journal of Clinical Investigation
Verified
Journal Article
Closed access
PDF file
MYMingcan Yu
Mingcan Yu
Subhashis PalSubhashis Pal
Subhashis Pal
CPCameron W. Paterson
Cameron W. Paterson
JLJau-Yi Li
Jau-Yi Li
ATAbdul Malik Tyagi
Abdul Malik Tyagi
RPRoberto Pacifici
Roberto Pacifici
Estrogen deficiency causes a gut microbiome–dependent expansion of BM Th17 cells and TNF-α–producing T cells. The resulting increased BM levels of IL-17a (IL-17) and TNF stimulate RANKL expression and activity, causing bone loss. However, the origin of BM Th17 cells and TNF+ T cells is unknown. Here, we show that ovariectomy (ovx) expanded intestinal Th17 cells and TNF+ T cells, increased their S1P receptor 1–mediated (S1PR1-mediated) egress from the intestine, and enhanced their subsequent influx into the BM through CXCR3- and CCL20-mediated mechanisms. Demonstrating the functional relevance of T cell trafficking, blockade of Th17 cell and TNF+ T cell egress from the gut or their influx into the BM prevented ovx-induced bone loss. Therefore, intestinal T cells are a proximal target of sex steroid deficiency relevant for bone loss. Blockade of intestinal T cell migration may represent a therapeutic strategy for the treatment of postmenopausal bone loss.

1 October 2018 in Nutrition
Verified
Journal Article
Closed access
HDHamid Y. Dar
Hamid Y. Dar
Subhashis PalSubhashis Pal
Subhashis Pal
PSPrashant Shukla
Prashant Shukla
Pradyumna Kumar MishraPradyumna Kumar Mishra
Pradyumna Kumar Mishra
GTGeetanjali B. Tomar
Geetanjali B. Tomar
RSRupesh K. Srivastava
Rupesh K. Srivastava

1 July 2015 in Biomaterials
Verified
Journal Article
Closed access
Jitendra Kumar TripathiJitendra Kumar Tripathi
Jitendra Kumar Tripathi
Subhashis PalSubhashis Pal
Subhashis Pal
BABhanupriya Awasthi
Bhanupriya Awasthi
AKAmit Kumar
Amit Kumar
ATAnshika Tandon
Anshika Tandon
JGJimut Kanti Ghosh
Jimut Kanti Ghosh

1 June 2019 in Cytokine
Verified
Journal Article
Closed access
RSRicha Shrivastava
Richa Shrivastava
MAMohammad Asif
Mohammad Asif
VSVarsha Singh
Varsha Singh
PDParul Dubey
Parul Dubey
SMShowkat Ahmad Malik
Showkat Ahmad Malik
SBSmrati Bhadauria
Smrati Bhadauria

1 February 2020 in Metabolism
Verified
Journal Article
Closed access
AGAnagha Ashok Gurjar
Anagha Ashok Gurjar
SKSapana Kushwaha
Sapana Kushwaha
SCSourav Chattopadhyay
Sourav Chattopadhyay
NDNabanita Das
Nabanita Das
Subhashis PalSubhashis Pal
Subhashis Pal
SSSabyasachi Sanyal
Sabyasachi Sanyal