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Photo of Dr. Dahia

Chitra Dahia, PhD

Photo of Dr. Dahia

Chitra Dahia, PhD

Back in the Game Patient Stories

Research Description

Spine Development and Regeneration Lab

The main focus of Dahia lab is to understand the role of major cell signaling pathways, particularly Shh, Wnt, BMP and TGFβ in postnatal development, differentiation, aging and degeneration of the intervertebral disc (IVD), and translate this to develop approaches for regeneration of the IVD and to treat lower back and disc related disorders.

Dahia researchIVDs are cartilagenous tissue present between each vertebra and its growth plates (GP). Each IVD consists of a central semi-liquid nucleus pulposus (NP), surrounded by a multi-layered annulus fibrosus (AF), and connected to the bodies of the adjacent vertebral bodies by cartilagenous end plates (EP). Together, these components form a strong joint that resists both tension and compression forces between vertebrae. Degenerative disc disease (DDD) is a major cause of lower back pain, and other neurological symptoms leading to a decreased quality of life. DDD is extremely common, affecting as many as one in seven people. However, how is it triggered is not known. The treatment costs are high, and often include surgical intervention. However, treatment is essentially palliative, since it treats the effects of disc degeneration rather than the causes.

Research in Dahia lab aims to identify the molecular mechanisms of postnatal growth, differentiation and aging of the IVD using mouse model system, and how these mechanisms are down-regulated, leading to age-related changes in the IVD. We have developed the mouse lumbar IVD as a model, and successfully shown that it can be used to identify the signaling pathways in the IVD that control postnatal growth and differentiation. We have found that during postnatal growth, the NP acts as a signaling center that controls both growth and differentiation of the postnatal IVD. NP cells express SHH, and blockade of Shh signaling both in vitro and in vivo shows that it is essential for cell proliferation and differentiation of the IVD. NP cells also express several WNT ligands, which are required to maintain Shh signaling in the IVD. Both these signaling pathways, and their downstream targets are down-regulated by the end of the growth period. Our studies show that Shh signaling, and the expression of differentiation markers, can be re-activated after the growth period by activation of canonical Wnt signaling. This suggests the potential of Shh and Wnt signaling pathways in regeneration of IVD.

The long-term goal is to identify potential biological approaches to therapy, using the same pathways that control IVD growth and differentiation during the early postnatal stages.

Candidates interested in PostDoctoral positions may email a detailed resume, electronic reprints of recent publications, and names and contact information for three references to dahiac@hss.edu

Selected Publications

Dahia CL, Iatridis JC, Risbud MV. (2018) New Horizons In Spine Research: Disc Biology, Tissue Engineering, Biomechanics, Translational And Clinical Research. JOR Spine. 2018; 1(3):1032. “Invited Perspective”

Seguin CA, Chan D, Dahia CL, Gazit Z. (2018) Latest advances in intervertebral disc development and progenitor cells. JOR spine. 2018; 1(3):1030. NIHMSID: NIHMS983739. “Invited Review Article”

Rajesh D, Dahia CL. (2018) Role of Sonic Hedgehog Signaling Pathway in Intervertebral Disk Formation and Maintenance. Current molecular biology reports. 2018. NIHMSID: NIHMS1510512. “Invited Review Article”

Bonavita R, Vincent K, Pinelli R, Dahia CL. (2018) Formation of the sacrum requires down-regulation of sonic hedgehog signaling in the sacral intervertebral discs. Biol Open. 2018 Jul 24;7(7). pii: bio035592. doi: 10.1242/bio.035592. PubMed PMID: 29784673; PubMed Central PMCID: PMC6078355.

Zheng HF*, Forgetta V*, Hsu YH*, Estrada K*, Rosello-Diez A*, Leo PJ*, Dahia CL*, et al., (2015) Whole-genome sequencing identifies EN1 as a determinant of bone density and fracture.Nature. 2015 Sep 14. doi: 10.1038/nature14878. [Epub ahead of print] PMID: 26367794
*These authors contributed equally to this work.

Winkler T, Mahoney E, Sinner D, Wylie C, Dahia CL. (2014) Wnt signaling activates Shh signaling in early postnatal intervertebral discs, and re-activates Shh signaling in old discs in the mouse. Accepted in PLoS One, Jun 3;9(6):e9844; PMID:24892825

Dahia CL*, Mahoney E, Wylie C*. (2012) Shh signaling from the nucleus pulposus is required for the postnatal growth and differentiation of the mouse intervertebral disc. PLoS ONE. 7(4): e35944. doi:10.1371/journal.pone.0035944 Epub 2012 Apr 27 * co-corresponding authors

Dahia CL, Mahoney E, Durrani A, Wylie C. (2011) Intercellular signaling pathways active during and after growth and differentiation of lumbar vertebral growth plate. Spine. Jun 15;36(14):1071-80.

Dahia CL, Sarkar MN, Rao AJ. (2011) A Comparative Analysis of Expression of Selected Genes during Induction of Differentiation in Neonatal Rats by Deprival of FSH or by Hyperthyroidism. The Open Andrology Journal. (3):14-24.

Dahia CL, Mahoney E, Durrani A, Wylie C. (2009) Postnatal growth, differentiation, and aging of the mouse intervertebral disc. Spine. Mar 1;34(5):447-55.

Dahia CL, Mahoney E, Durrani A, Wylie C. (2009) Intercellular signaling pathways active during intervertebral disc growth, differentiation and aging. Spine. Mar 1;34(5):456-62.

Dahia CL, Rao AJ. (2009) Identification of Intracisternal A-Particle-Like Element as an FSH- regulated Transcript in Immature Rat Sertoli Cells. The Open Andrology Journal. (1):10-19.

Dahia CL, Petruz P, Hall SH, Rao AJ. (2008) Effect of deprivation of endogenous follicle stimulating hormone on rat epididymis: a histological evaluation. Reproductive BioMedicine Online. Sep;17(3) 331-7.

Dahia CL, Rao AJ. (2006) Demonstration of follicle-stimulating hormone receptor in cauda epididymis of rat. Biology of Reproduction. Jul;75(1):98-106.

Dahia CL, Rao AJ. (2006) Regulation of FSH receptor, PKIbeta, IL-6 and calcium mobilization: Possible mediators of differential action of FSH. Molecular and Cellular Endocrinology. Mar 9;247(1-2):73-81.


Assistant Scientist, Tissue Engineering, Regeneration and Repair Program, Hospital for Special Surgery

Assistant Professor, Department of Cell and Developmental Biology, Weill Cornell Medical College