Rohan Bhattacharya

We mapped the whole human fallopian tube in 3D and at single-cell resolution via our CODA workflow.

More about this work here: biorxiv.org/content/10.1...

Our recent observations are distinct from conventional active matter. Self-propelled colloidal particles neither secrete inhibitory molecules, nor actively modulate adhesion molecules, which are two key ingredients leading to our observed patterned aggregates.

Here: www.nature.com/articles/s41...

Ahead of #KidneyWk25,
I’m recruiting 2-3 folks to help us map the genomics of pediatric kidney diseases toward treatments & cures. Please reach out if you’d like to connect in Houston @bostonchildrens.bsky.social @asnkidney.bsky.social @harvardmed.bsky.social @broadinstitute.org
sampsonlab.org

Engineered human induced pluripotent stem cell models reveal altered podocytogenesis in congenital heart disease-associated SMAD2 mutations - Nature Biomedical Engineering This study investigates the role of SMAD2 genetic variants associated with congenital heart disease on renal development using a CRISPR-engineered human induced pluripotent stem cell model on a microp...

Read our full paper in @natbiomedeng.nature.com:
www.nature.com/articles/s41...

Because murine SMAD2 loss is embryonically lethal, we leveraged CRISPR-edited human iPS cells and organ-on-chip platforms to model human-specific developmental mechanisms.
These systems enabled functional and molecular dissection of SMAD2-dependent pathways in podocytogenesis.

These findings revealed how pathogenic SMAD2 mutations impair glomerular morphogenesis, disrupt podocyte–endothelial cross-talk, and ultimately affect organ-level filtration function.

We next integrated mutant and isogenic control podocytes with endothelial cells in a microengineered glomerulus-on-a-chip system.
Mutant chips displayed extensive cell delamination and increased albumin leakage, reflecting compromised glomerular barrier integrity.

Upon podocyte differentiation, SMAD2 mutant cells failed to form mature foot processes, exhibited reduced expression of lineage markers, and adopted a mesenchymal phenotype, indicating a loss of terminal differentiation potential.

We found that pathogenic SMAD2 mutations disrupt mesoderm commitment, leading to a skewed differentiation pathway toward the posterior mesoderm.
Mutant intermediate mesoderm (IM) cells show enhanced motility, mesenchymal features, upregulate EMT markers, and undergo necroptosis.

Variants in CHD-associated genes often lead to multisystem developmental abnormalities, including kidney malformations.
Given the strong association between SMAD2-mediated CHD and chronic kidney disease (CKD), we investigated how SMAD2 mutations affect podocytogenesis & function.

This has been an incredible collaboration with #TarshaWard, #ChristineSeidman, #JonathanSeidman from @harvardmed.bsky.social, and huge thanks to my Ph.D. advisor @stemcellengineer.bsky.social, the #MusahLab members #LolaKalejaiye, #AlekMishra, #SophiaLeeman, #Hamidreza for making this work possible.

Thrilled to share that a part of my Ph.D. work from
@dukeubme.bsky.social @stemcellengineer.bsky.social Lab is now out in @natbiomedeng.nature.com!
We investigated the impact of CHD-linked SMAD2 variants on kidney development using engineered human iPS cells in a microphysiological system.

Doug Wassarman of Dana-Farber Cancer Institute

New research published in @science.org led by @danafarber.bsky.social’s Doug Wassarman and @kranzuschlab.bsky.social reveals new protein chemistry named deazaguanylation that controls activation of immunity.

Read more: bit.ly/3WeKsLb

Get by with a little help from my friends (esp @rohanbme.bsky.social) 💕💕

Thanks to @stemcellengineer.bsky.social for visiting us at Cedars-Sinai last week! She’s doing amazing work developing advanced kidney-on-chip systems and much more.