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Pericytes are organ-specific regulators of tissue morphogenesis.

Overview

  1. Department of Tissue Morphogenesis, Max Planck Institute for Molecular Biomedicine,Münster, Germany
  2. Max Planck Institute for Molecular Biomedicine, Bioinformatics Service Unit,Münster, Germany
  3. Department of Vascular Cell Biology, Max Planck Institute for Molecular Biomedicine,Münster, Germany
  4. Vascular Patterning Dynamics Group, Max Planck Institute for Molecular Biomedicine,Münster, Germany
Journal: Nature communications, volume 17, issue 1, article 4229
Dates: received 16 January 2025; accepted 27 March 2026; published online 12 May 2026
Type: Research article · Language: English
License: CC BY
Identifiers: DOI 10.1038/s41467-026-71643-1 · PMID 42120366 · PMCID PMC13168628 · OpenAlex W7160937948
Open access: gold, a free copy (OpenAlex)
Status: code verified
Categories: mouse (organism), cellular / molecular (subfield)
Methods: Spectral & time-frequency, Statistics, Smoothing, state filtering, decompositions, Evoked potentials, Connectivity, Machine learning, fMRI & imaging, Physiology & signal measures
Keywords: Organogenesis, Angiogenesis, Mouse
MeSH: Brain*, Lung*, Morphogenesis*, Pericytes*, Animals, Astrocytes, Endothelial Cells, Hepatocyte Growth Factor, Mice, Mice, Knockout, Organ Specificity, Paracrine Communication (* major topic)
Topic: Barrier Structure and Function Studies (Neurology, Neuroscience), according to OpenAlex
Funding: Deutsche Forschungsgemeinschaft (DFG) (CRC 1366, project no. 394046768); Max Planck Society
Citations: not cited yet (Europe PMC); 136 references in the paper

Abstract

Endothelial cells lining the vessel network are indispensable for vascular transport but also provide paracrine signals controlling the behavior of nearby cell types. Pericytes are another essential component of the vessel wall, but little is known about their interactions with other cell populations during organ growth and patterning. Here, we use mouse genetics to address the function of three pericyte-derived factors in postnatal lung and brain. We find that inactivation of the gene for hepatocyte growth factor (HGF) or brain-derived neurotrophic factor (BDNF) in pericytes causes no overt alterations in postnatal brain but impairs lung development, which we attribute to defective interaction with AT2 epithelial cells and pulmonary endothelium, respectively. In contrast, pericyte expression of the growth factor Nodal is dispensable for lung morphogenesis but regulates vessel growth and barrier function in the postnatal brain through interactions with endothelial cells, astrocytes and microglia. Taken together, our findings establish that pericytes are a critical source of paracrine signals controlling morphogenetic processes in an organ-specific fashion.

Reproduced under the paper's license (CC BY), from the paper cited above.

Code

No file of the authors' code could be read here: it is described below, and read at its source.

keeper.mpdl.mpg.de/d/301c44f11ccb455ab199

License: none: the authors keep all their rights
State: the link answers, verified on 28 September 2026
Evidence: the link answers
Software Heritage: not checked
Found in: “Code availability”
Not found: README, license file, CITATION.cff, environment file, tests, continuous integration, documentation
Availability: 1 check, the latest on 28 September 2026: the link answers (HTTP 200)
  • 28 September 2026: the link answers (HTTP 200)

Bioinformatics-Service-MPI-Munster

License: none: the authors keep all their rights
State: the link answers, verified on 28 September 2026
Evidence: the link answers
Software Heritage: not checked
Found in: “Code availability”
Not found: README, license file, CITATION.cff, environment file, tests, continuous integration, documentation
Availability: 1 check, the latest on 28 September 2026: the link answers (HTTP 200)
  • 28 September 2026: the link answers (HTTP 200)

Code availability

Custom code for scRNA-seq analysis, based on existing packages and own contributions, is publicly available at https://keeper.mpdl.mpg.de/d/301c44f11ccb455ab199/. Dependencies “scrna-tools” and “anndataview” can be found at https://github.com/Bioinformatics-Service-MPI-Munster.

Reproduced under the paper's license (CC BY), from the paper cited above.

Tracing map

Proposed by the machine: these links were found in the paper and verified at the source, without human review. The map will receive a Zenodo DOI once one of the paper's authors has validated it with their ORCID.

What the map holds:

  • 2 repositories of the authors' code, each at its verified commit, with its license and how the link was found in the paper;
  • 0 scripts, each with its path and the digest of its content;
  • no match between paragraphs and code yet;
  • neither the text of the paper nor the code itself.

Its JSON (tracing-map.json) is deposited on Zenodo with its DOI once the map is validated.

Data

Datasets cited

Data availability

The scRNA-seq data generated in this study have been deposited in the Gene Expression Omnibus under accession number GSE285933 (https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE285933). The mouse reference genome GRCm39 with GENCODE M26 annotation (https://www.gencodegenes.org/mouse/release_M26.html) was used for mapping the reads in this study. All other relevant data supporting the key findings of this study are available within the article and its Supplementary Information files. All measurements used for quantification are provided in the Source Data file along with the results of the different statistical analyses performed. Source data are provided with this paper. All individual mouse lines used in this study are commercially available at The Jackson Laboratory or through the lead author. All other biological materials described in this article are available through commercial suppliers as indicated. Source data are provided with this paper.

Reproduced under the paper's license (CC BY), from the paper cited above.

Versions

The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.

Version 1, 28 September 2026: the first record

Recorded: type, language, journal, volume, issue, pages, dates, 7 authors, 3 keywords, 12 MeSH terms, 2 funders, 135 references.

Cite

This paper

Rasouli, S. J., Kruse, K., Diéguez-Hurtado, R., Ghanbari, P., Aravamudhan, A., Pitulescu, M. E., & Adams, R. H. (2026). Pericytes are organ-specific regulators of tissue morphogenesis. Nature communications, 17(1), 4229. https://doi.org/10.1038/s41467-026-71643-1

BibTeX

@article{rasouli2026pericytes,
author = {Rasouli, Seyed Javad and Kruse, Kai and Diéguez-Hurtado, Rodrigo and Ghanbari, Parisa and Aravamudhan, Anusha and Pitulescu, Mara E. and Adams, Ralf H.},
title = {{Pericytes are organ-specific regulators of tissue morphogenesis}},
journal = {Nature communications},
year = {2026},
month = may,
volume = {17},
number = {1},
pages = {4229},
publisher = {Nature Publishing Group},
issn = {2041-1723},
doi = {10.1038/s41467-026-71643-1},
url = {https://doi.org/10.1038/s41467-026-71643-1},
pmid = {42120366},
pmcid = {PMC13168628}
}

RIS

TY - JOUR
AU - Rasouli, Seyed Javad
AU - Kruse, Kai
AU - Diéguez-Hurtado, Rodrigo
AU - Ghanbari, Parisa
AU - Aravamudhan, Anusha
AU - Pitulescu, Mara E.
AU - Adams, Ralf H.
TI - Pericytes are organ-specific regulators of tissue morphogenesis
T2 - Nature communications
J2 - Nat Commun
PY - 2026
DA - 2026/05/12
VL - 17
IS - 1
SP - 4229
SN - 2041-1723
PB - Nature Publishing Group
DO - 10.1038/s41467-026-71643-1
UR - https://doi.org/10.1038/s41467-026-71643-1
LA - en
ER -

CSL-JSON

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