Baohong Zhao

Many skeletal diseases are largely associated with or caused by inflammation. However, the underlying mechanisms are far from understood. Our lab studies osteoimmunology, an interdisciplinary field linking bone biology and the immune system, focusing on inflammatory regulation of gene expression and signaling in macrophage differentiation to osteoclasts (see the model of a new molecular regulatory network we recently identified), adipogenesis, skeletal damage and repair involved in disease (such as osteoporosis and inflammatory arthritis). 

We equip genetic approaches (knockout and transgenic mice), primary cells (for example, bone marrow cells and PBMCs), a combination of molecular and cellular methods, various next-generation techniques (RNAseq, ATACseq, ChIP-seq, scRNAseq), multi-omics approaches, and disease models (such as RA, osteoporosis, fracture, high fat diet-induced obesity/type-2 diabetes mouse models). We work extensively on signal transduction and crosstalk, genetic and epigenetic regulation of gene transcription and function, cell differentiation and in vivo bone remodeling and metabolism. 

We are dedicated to advancing scientific knowledge addressing how the immune system regulates the skeleton and identifying novel therapeutic targets for improving musculoskeletal diseases associated with inflammation.

Skeletal diseases are largely associated with or caused by inflammation. However, the underlying mechanisms are far from understood. Our lab studies osteoimmunology, an interdisciplinary field linking bone biology and the immune system, focusing on inflammatory regulation of gene expression and signaling in macrophage differentiation to osteoclasts (see the model of a new molecular regulatory network we recently identified), adipogenesis, skeletal damage and repair involved in disease (such as osteoporosis and inflammatory arthritis). 

We equip genetic approaches (knockout and transgenic mice), primary cells (for example, bone marrow cells and PBMCs), a combination of molecular and cellular methods, various next-generation techniques (RNAseq, ATACseq, ChIP-seq, scRNAseq), multi-omics approaches, and disease models (such as RA, osteoporosis, fracture, high fat diet-induced obesity/type-2 diabetes mouse models). 

We work extensively on signal transduction and crosstalk, genetic and epigenetic regulation of gene transcription and function, cell differentiation and in vivo bone remodeling and metabolism. We are dedicated to advancing scientific knowledge addressing how the immune system regulates the skeleton and identifying novel therapeutic targets for improving musculoskeletal diseases associated with inflammation. 

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