𝗛𝗼𝘄 𝗱𝗼𝗲𝘀 𝗮 𝘀𝗸𝗶𝗻 𝘀𝘁𝗲𝗺 𝗰𝗲𝗹𝗹 𝗸𝗻𝗼𝘄 𝘁𝗼 𝗿𝗲𝗺𝗮𝗶𝗻 𝗮 𝘀𝘁𝗲𝗺 𝗰𝗲𝗹𝗹? Our latest study, now published in the 𝘾𝙚𝙡𝙡 𝘾𝙤𝙢𝙢𝙪𝙣𝙞𝙘𝙖𝙩𝙞𝙤𝙣 𝙖𝙣𝙙 𝙎𝙞𝙜𝙣𝙖𝙡𝙞𝙣𝙜, uncovers an unexpected mechanism linking the extracellular environment to the maintenance of keratinocyte stemness.
Johan Ajnabi
@johanajnabi.com
PhD Candidate | Mechanobiology • Epigenetics • Regenerative Biology | Institute for Stem Cell Science and Regenerative Medicine (inStem) | Seeking Postdoctoral Opportunities (2026-27) More about me: https://johanajnabi.com
Honored to see our recent preprint featured by the Epithelial Mechanics Fan Club. We explore how wound-induced actin remodeling drives ERK inactivation and DNMT3a localization linking epithelial mechanics to epigenetic regulation during repair. I would love to hear your thoughts and feedback. 👇
epithelial mechanics fan club@epimechfc.bsky.social · 3mo agoAjnabi, J., Dam, B., Gupta, E., Saha, T., Dutta, A., Kumar, S., ... & Jamora, C. (2026). Actin-dependent mechanotransduction controls nucleocytoplasmic partitioning of DNMT3a through ERK1/2 signaling during cutaneous wound healing. bioRxiv, 2026-01. #EpithelialMechanics buff.ly/xkUWazo
Excited to see this work from our lab featured by the Epithelial Mechanics Fan Club. This study explores how epithelial tissues respond to injury through dynamic changes in signaling, mechanics, and cellular state. Many of the questions raised here went on to inspire aspects of my own research. 👇
epithelial mechanics fan club@epimechfc.bsky.social · 3mo agoBhatt, T., Dey, R., Hegde, A., Ketkar, A. A., Pulianmackal, A. J., Deb, A. P., Rampalli, S., & Jamora, C. (2022). Initiation of wound healing is regulated by the convergence of mechanical and epigenetic cues. PLoS biology, 20(9), e3001777. #EpithelialMechanics buff.ly/UMwJF6h
Special thanks to @juliaeckert.bsky.social and @onenimesa.bsky.social for giving me the opportunity to express my thoughts and communicate my discoveries, and highlighting me as delegate. Happy to be part of @epimechfc.bsky.social community.
epithelial mechanics fan club@epimechfc.bsky.social · 2mo agoWound repair is more than simply closing a gap in the tissue. Mechanical injury rapidly reshapes signaling, nuclear organization, and cellular identity across the epithelium. I'm @johanajnabi.com, and here are studies that changed how I think about epithelial wound healing. bsky.app/profile/epim...
I wrote this thread to explore how epithelial tissues reinterpret mechanical injury through signaling rewiring, cytoskeletal remodeling, and epigenetic plasticity during wound repair. Would love to hear your thoughts and discussions 👇
epithelial mechanics fan club@epimechfc.bsky.social · 2mo agoWound repair is more than simply closing a gap in the tissue. Mechanical injury rapidly reshapes signaling, nuclear organization, and cellular identity across the epithelium. I'm @johanajnabi.com, and here are studies that changed how I think about epithelial wound healing. bsky.app/profile/epim...
Happy to collaborate with my colleague @abhikdutta.bsky.social on this fantastic work: linkedin.com/posts/johana... #Vitiligo #SpatialTranscriptomics #Dermatology #Collaboration #Immunology #TranslationalResearch
Clinical & Translational Immunology | ASI Journal | Wiley Online Library | Johan Ajnabi
Happy to collaborate with my colleague Abhik Dutta on this fantastic work. This project pushed me to think about disease and treatment at the level of tissue architecture. Vitiligo is clearly shaped ...
linkedin.com
1/6: Over the past few weeks, I stepped outside the lab and tried something new: I built my academic website from scratch. I had only a very preliminary understanding of HTML — so this was… an adventure.
Meet the one-eyed mechanobiology monster. Turns out cells look terrifying when you zoom in far enough. 👾🔬 #microscopy #alien #monster #mechanobiology #CellBiology #confocal #imaging #immunofluorescence
Signaling depends not just on interactions, but on location. In our recent study led by @binitadam.bsky.social, we show that Mindin-αM integrin signaling requires trafficking to acidic early endosomes, where pH-driven integrin conformational changes enable STAT3 activation and stemness. #signaling
bioRxiv Cell Biology@biorxiv-cellbio.bsky.social · 11mo agoMindin-α-M-Integrin endocytosis activates STAT3 to maintain keratinocyte stemness https://www.biorxiv.org/content/10.1101/2025.08.24.669246v1
Feed: "JCI Insight -- New Articles" By: Sunny Kataria, Isha Rana, Krithika Badarinath, Rania F. Zaarour, Gaurav Kansagara, Sultan Ahmed, Abrar Rizvi, Dyuti Saha, Binita Dam, Abhik Dutta, Ravindra K. Zirmire, Edries Yousaf Hajam, Pankaj Kumar, Akash Gulyani, Colin Jamora
Mindin regulates fibroblast subpopulations through distinct Src family kinases during fibrogenesis
Fibrosis results from excessive extracellular matrix (ECM) deposition, which causes tissue stiffening and organ dysfunction. Activated fibroblasts, central to fibrosis, exhibit increased migration, proliferation, contraction, and ECM production. However, it remains unclear if the same fibroblast performs all of the processes that fall under the umbrella term of “activation.” Owing to fibroblast heterogeneity in connective tissues, subpopulations with specific functions may operate under distinct regulatory controls. Using a transgenic mouse model of skin fibrosis, we found that Mindin (also known as spondin-2), secreted by Snail-transgenic keratinocytes, differentially regulates fibroblast subpopulations. Mindin promotes migration and inflammatory gene expression in SCA1+ dermal fibroblasts via Fyn kinase. In contrast, it enhances contractility and collagen production in papillary CD26+ fibroblasts through c-Src signaling. Moreover, in the context of the fibrotic microenvironment of the tumor stroma, we found that differential responses of resident fibroblast subpopulations to Mindin extend to the generation of functionally heterogeneous cancer-associated fibroblasts. This study identifies Mindin as a key orchestrator of dermal fibroblast heterogeneity, reshaping cellular dynamics and signaling diversity in the complex landscapes of skin fibrosis and cancer.
insight.jci.org
Behind-the-scenes: Dr. Dyuti Saha at the confocal microscope at the Core Imaging Facility in the Department of Life Sciences and Shiv Nadar University (an Institution of Eminence) capturing images of the vasculature in the fibrotic skin.
Journal of Clinical Investigation@jci.org · last yr.Vasculopathy occurs early in systemic sclerosis, but intervention strategies are lacking. Colin Jamora & team reveal ANGPTL2 as an inducer of vasculopathy that drives cutaneous fibrogenesis in mice—mirroring SSc—and present a therapueutic approach: UAS03: buff.ly/SpOiuCc
ICYMI: Vasculopathy occurs early in systemic sclerosis, but intervention strategies are lacking. Colin Jamora & team reveal ANGPTL2 as an inducer of vasculopathy that drives cutaneous fibrogenesis in mice—mirroring SSc—and present a therapeutic approach: UAS03. buff.ly/xNYvnRj
Vasculopathy occurs early in systemic sclerosis, but intervention strategies are lacking. Colin Jamora & team reveal ANGPTL2 as an inducer of vasculopathy that drives cutaneous fibrogenesis in mice—mirroring SSc—and present a therapueutic approach: UAS03: buff.ly/SpOiuCc
Actin-dependent mechanotransduction controls nucleocytoplasmic partitioning of DNMT3a through ERK1/2 signaling during cutaneous wound healing https://www.biorxiv.org/content/10.64898/2026.01.15.699481v1
How do mechanical cues at wounds reprogram skin cells? Our new study shows that actin remodeling regulates ERK1/2 signaling to allow DNMT3a nuclear entry, linking mechanotransduction to epigenetic control in early wound healing. #Mechanobiology #Epigenetics #WoundHealing #bioRxiv
bioRxiv Cell Biology@biorxiv-cellbio.bsky.social · 7mo agoActin-dependent mechanotransduction controls nucleocytoplasmic partitioning of DNMT3a through ERK1/2 signaling during cutaneous wound healing https://www.biorxiv.org/content/10.64898/2026.01.15.699481v1