Mindin (SPON2) Is Essential for Cutaneous Fibrogenesis in a Mouse Model of Systemic Sclerosis

Isha Rana, Sunny Kataria, Tuan Lin Tan, Edries Yousaf Hajam, Deepak Kumar Kashyap, Dyuti Saha, Johan Ajnabi, Sayan Paul, Shashank Jayappa, Akhil S.H.P. Ananthan, Pankaj Kumar, Rania F. Zaarour, J. Haarshaadri, Gaurav Kansagara, Abrar Rizvi, Ravindra K. Zirmire, Krithika Badarinath, Sneha Uday Khedkar, Yogesh Chandra, Rekha SamuelRenu George, Debashish Danda, Paul Mazhuvanchary Jacob, Rakesh Dey, Perundurai S. Dhandapany, You Wen He, John Varga, Shyni Varghese, Colin Jamora

Research output: Contribution to journalArticlepeer-review

3 Scopus citations


Systemic sclerosis is a fibrotic disease that initiates in the skin and progresses to internal organs, leading to a poor prognosis. Unraveling the etiology of a chronic, multifactorial disease such as systemic sclerosis has been aided by various animal models that recapitulate certain aspects of the human pathology. We found that the transcription factor SNAI1 is overexpressed in the epidermis of patients with systemic sclerosis, and a transgenic mouse recapitulating this expression pattern is sufficient to induce many clinical features of the human disease. Using this mouse model as a discovery platform, we have uncovered a critical role for the matricellular protein Mindin (SPON2) in fibrogenesis. Mindin is produced by SNAI1 transgenic skin keratinocytes and aids fibrogenesis by inducing early inflammatory cytokine production and collagen secretion in resident dermal fibroblasts. Given the dispensability of Mindin in normal tissue physiology, targeting this protein holds promise as an effective therapy for fibrosis.

Original languageEnglish (US)
Pages (from-to)699-710.e10
JournalJournal of Investigative Dermatology
Issue number5
StatePublished - May 2023
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Dermatology
  • Cell Biology


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