Nazir M. Khan
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Nazir M. Khan has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
- Hicham Drissi
Department of Orthopaedics Emory University School of Medicine Atlanta Georgia USA
1 shared publication - Hiroshi Yamada
Department of Orthopaedic Surgery, Wakayama Medical University, Wakayama, Japan
1 shared publication - Katrin Henke
Department of Orthopaedics, Emory University School of Medicine , Atlanta, GA 30329
1 shared publication - Kimihide Murakami
Department of Orthopaedics, Emory University, Atlanta, GA 30329, USA
1 shared publication - Martha Elena Diaz‐Hernandez
Department of Orthopaedics, Emory University, Atlanta, GA 30329, USA
1 shared publication - Shizumasa Murata
Department of Orthopaedics, Emory University, Atlanta, GA 30329, USA
1 shared publication
Latest Publications
- Open Access
Inhibition of KDM2/7 Promotes Notochordal Differentiation of hiPSCs
Intervertebral disc disease (IDD) is a debilitating spine condition that can be caused by intervertebral disc (IVD) damage which progresses towards IVD degeneration and dysfunction. Recently, human pluripotent stem cells (hPSCs) were recognized as a valuable resource for cell-based regenerative medicine in skeletal diseases. Therefore, adult somatic cells reprogrammed into human induced pluripotent stem cells (hiPSCs) represent an attractive cell source for the derivation of notochordal-like cells (NCs) as a first step towards the development of a regenerative therapy for IDD. Utilizing a differentiation method involving treatment with a four-factor cocktail targeting the BMP, FGF, retinoic acid, and Wnt signaling pathways, we differentiate CRISPR/Cas9-generated mCherry-reporter knock-in hiPSCs into notochordal-like cells. Comprehensive analysis of transcriptomic changes throughout the differentiation process identified regulation of histone methylation as a pivotal driver facilitating the differentiation of hiPSCs into notochordal-like cells. We further provide evidence that specific inhibition of histone demethylases KDM2A and KDM7A/B enhanced the lineage commitment of hiPSCs towards notochordal-like cells. Our results suggest that inhibition of KDMs could be leveraged to alter the epigenetic landscape of hiPSCs to control notochord-specific gene expression. Thus, our study highlights the importance of epigenetic regulators in stem cell-based regenerative approaches for the treatment of disc degeneration.
Open AccessInhibition of KDM2/7 Promotes Notochordal Differentiation of hiPSCs
Intervertebral disc disease (IDD) is a debilitating spine condition that can be caused by intervertebral disc (IVD) damage which progresses towards IVD degeneration and dysfunction. Recently, human pluripotent stem cells (hPSCs) were recognized as a valuable resource for cell-based regenerative medicine in skeletal diseases. Therefore, adult somatic cells reprogrammed into human induced pluripotent stem cells (hiPSCs) represent an attractive cell source for the derivation of notochordal-like cells (NCs) as a first step towards the development of a regenerative therapy for IDD. Utilizing a differentiation method involving treatment with a four-factor cocktail targeting the BMP, FGF, retinoic acid, and Wnt signaling pathways, we differentiate CRISPR/Cas9-generated mCherry-reporter knock-in hiPSCs into notochordal-like cells. Comprehensive analysis of transcriptomic changes throughout the differentiation process identified regulation of histone methylation as a pivotal driver facilitating the differentiation of hiPSCs into notochordal-like cells. We further provide evidence that specific inhibition of histone demethylases KDM2A and KDM7A/B enhanced the lineage commitment of hiPSCs towards notochordal-like cells. Our results suggest that inhibition of KDMs could be leveraged to alter the epigenetic landscape of hiPSCs to control notochord-specific gene expression. Thus, our study highlights the importance of epigenetic regulators in stem cell-based regenerative approaches for the treatment of disc degeneration.