Nestin/CXCL12 immunohistochemistry and RNA sequencing map the bone marrow microenvironment in aplastic anemia.

Astrid Beerlage, Carl P Zinner, Jakob R Passweg, Beatrice Drexler, Alexandar Tzankov

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Article in Disease models & mechanisms, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

5 authors.

Astrid BeerlageDivision of Hematology, University Hospital Basel, University of Basel, 4031 Basel, Switzerland.ORCID 0000-0002-0143-544X

Carl P ZinnerInstitute of Medical Genetics and Pathology, University Hospital Basel, University of Basel, 4031 Basel, Switzerland.ORCID 0000-0003-1609-0920

Jakob R PasswegDivision of Hematology, University Hospital Basel, University of Basel, 4031 Basel, Switzerland.ORCID 0000-0001-7092-3351

Beatrice DrexlerDivision of Hematology, University Hospital Basel, University of Basel, 4031 Basel, Switzerland.ORCID 0000-0002-7046-0825

Alexandar TzankovInstitute of Medical Genetics and Pathology, University Hospital Basel, University of Basel, 4031 Basel, Switzerland.ORCID 0000-0002-1100-3819

Funding

Universität Basel

6 · The paper itself

Abstract

Aplastic anemia (AA) is a rare bone marrow failure syndrome characterized by immune-mediated destruction of hematopoietic stem and progenitor cells (HSPCs). The contribution of the bone marrow microenvironment remains incompletely understood. Here, we analyzed 29 bone marrow biopsies from patients with moderate (mAA), severe (sAA) and very severe (vsAA) AA, along with 12 unaffected controls and seven subcortical pseudohypocellular samples. Immunohistochemistry for nestin and CXCL12 was performed to quantify stromal niches. RNA sequencing was carried out to investigate immune and niche-related gene expression patterns. Patients with sAA exhibited a significantly increased number of nestin+ niches compared to patients with mAA and controls. CXCL12+ niches showed no significant differences between groups. RNA sequencing revealed upregulation of immune response genes, as well as pathways related to interferon-gamma signaling, JAK-STAT3 activation and antigen presentation. Downregulated genes and pathways pointed to impaired DNA repair, cell cycle regulation and epigenetic stability. Our findings support a model in which AA pathogenesis is driven by immune injury and compensatory, yet dysfunctional, stromal remodeling. These data underline the importance of the bone marrow microenvironment in AA.

Indexed as

Anemia, AplasticBone MarrowCellular MicroenvironmentChemokine CXCL12NestinSequence Analysis, RNAFemaleGene Expression RegulationHumansImmunohistochemistryMaleSignal TransductionStem Cell NicheChemokine CXCL12CXCL12 protein, humanNestinAplastic anemiaBone marrow microenvironmentBone marrow nicheCXCL12Nestin

Identifiers

PMID41943582

DOI10.1242/dmm.052564

PMCPMC13225205

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.