{"entity": "researcher", "timestamp": "2026-07-20T22:34:48.033Z", "family": "Johansson", "given": "Martin E", "initials": "ME", "orcid": "0000-0001-8510-3102", "affiliations": ["Clinical Pathology Sahlgrenska University Hospital  Gothenburg Sweden", "Institute of Biomedicine, Department of Laboratory Medicine University of Gothenburg  Gothenburg Sweden", "The Sahlgrenska Cancer Center University of Gothenburg  Gothenburg Sweden"], "links": {"self": {"href": "https://publications.scilifelab.se/researcher/b85588d272854ff2a9d6c4e364529971.json"}, "display": {"href": "https://publications.scilifelab.se/researcher/b85588d272854ff2a9d6c4e364529971"}}, "publications": [{"entity": "publication", "iuid": "11c43093eed24cf3b53703e7743aab32", "links": {"self": {"href": "https://publications.scilifelab.se/publication/11c43093eed24cf3b53703e7743aab32.json"}, "display": {"href": "https://publications.scilifelab.se/publication/11c43093eed24cf3b53703e7743aab32"}}, "title": "The injury-induced transcription factor SOX9 alters the expression of LBR, HMGA2, and HIPK3 in the human kidney.", "authors": [{"family": "Kha", "given": "Michelle", "initials": "M"}, {"family": "Krawczyk", "given": "Krzysztof", "initials": "K"}, {"family": "Choong", "given": "Oi Kuan", "initials": "OK", "orcid": "0000-0003-0257-4748", "researcher": {"href": "https://publications.scilifelab.se/researcher/57045fc513524ab2947dd9f24bac0838.json"}}, {"family": "De Luca", "given": "Francesco", "initials": "F"}, {"family": "Altiparmak", "given": "G\u00fclay", "initials": "G"}, {"family": "K\u00e4llberg", "given": "Eva", "initials": "E"}, {"family": "Nilsson", "given": "Hel\u00e9n", "initials": "H"}, {"family": "Leandersson", "given": "Karin", "initials": "K", "orcid": "0000-0001-8254-3137", "researcher": {"href": "https://publications.scilifelab.se/researcher/4736923f382845c2990efb251340bfb4.json"}}, {"family": "Sw\u00e4rd", "given": "Karl", "initials": "K", "orcid": "0000-0002-7255-5510", "researcher": {"href": "https://publications.scilifelab.se/researcher/b6bf44f11b9d4029bf4bb06ffee09e8c.json"}}, {"family": "Johansson", "given": "Martin E", "initials": "ME", "orcid": "0000-0001-8510-3102", "researcher": {"href": "https://publications.scilifelab.se/researcher/b85588d272854ff2a9d6c4e364529971.json"}}], "type": "journal article", "published": "2023-01-01", "journal": {"title": "Am. J. Physiol. Renal Physiol.", "issn": "1522-1466", "volume": "324", "issue": "1", "pages": "F75-F90", "issn-l": "1522-1466"}, "abstract": "Induction of SRY box transcription factor 9 (SOX9) has been shown to occur in response to kidney injury in rodents, where SOX9-positive cells proliferate and regenerate the proximal tubules of injured kidneys. Additionally, SOX9-positive cells demonstrate a capacity to differentiate toward other nephron segments. Here, we characterized the role of SOX9 in normal and injured human kidneys. SOX9 expression was found to colocalize with a proportion of so-called scattered tubular cells in the uninjured kidney, a cell population previously shown to be involved in kidney injury and regeneration. Following injury and in areas adjacent to inflammatory cell infiltrates, SOX9-positive cells were increased in number. With the use of primary tubular epithelial cells (PTECs) obtained from human kidney tissue, SOX9 expression was spontaneously induced in culture and further increased by transforming growth factor-\u03b21, whereas it was suppressed by interferon-\u03b3. siRNA-mediated knockdown of SOX9 in PTECs followed by analysis of differential gene expression, immunohistochemical expression, and luciferase promoter assays suggested lamin B receptor (LBR), high mobility group AT-hook 2 (HMGA2), and homeodomain interacting protein kinase 3 (HIPK3) as possible target genes of SOX9. Moreover, a kidney explant model was used to demonstrate that only SOX9-positive cells survive the massive injury associated with kidney ischemia and that the surviving SOX9-positive cells spread and repopulate the tubules. Using a wound healing assay, we also showed that SOX9 positively regulated the migratory capacity of PTECs. These findings shed light on the functional and regulatory aspects of SOX9 activation in the human kidney during injury and regeneration.NEW & NOTEWORTHY Recent studies using murine models have shown that SRY box transcription factor 9 (SOX9) is activated during repair of renal tubular cells. In this study, we showed that SOX9-positive cells represent a proportion of scattered tubular cells found in the uninjured human kidney. Furthermore, we suggest that expression of LBR, HMGA2, and HIPK3 is altered by SOX9 in the kidney tubular epithelium, suggesting the involvement of these gene products in kidney injury and regeneration.", "doi": "10.1152/ajprenal.00196.2022", "pmid": "36454702", "labels": {"Clinical Genomics Lund": "Service", "Clinical Genomics Gothenburg": "Service", "Clinical Genomics": "Service"}, "xrefs": [], "notes": [], "created": "2023-02-20T13:56:14.537Z", "modified": "2023-11-30T22:32:49.212Z"}, {"entity": "publication", "iuid": "1ad131dd022d484f84ca9b9dcb288a09", "links": {"self": {"href": "https://publications.scilifelab.se/publication/1ad131dd022d484f84ca9b9dcb288a09.json"}, "display": {"href": "https://publications.scilifelab.se/publication/1ad131dd022d484f84ca9b9dcb288a09"}}, "title": "Features of increased malignancy in eosinophilic clear cell renal cell carcinoma.", "authors": [{"family": "Nilsson", "given": "Hel\u00e9n", "initials": "H"}, {"family": "Lindgren", "given": "David", "initials": "D"}, {"family": "Axelson", "given": "H\u00e5kan", "initials": "H"}, {"family": "Brueffer", "given": "Christian", "initials": "C", "orcid": "0000-0002-3826-0989", "researcher": {"href": "https://publications.scilifelab.se/researcher/6bf6758bd7a54626bdf3b82888431296.json"}}, {"family": "Saal", "given": "Lao H", "initials": "LH"}, {"family": "Lundgren", "given": "Jaana", "initials": "J"}, {"family": "Johansson", "given": "Martin E", "initials": "ME", "orcid": "0000-0001-8510-3102", "researcher": {"href": "https://publications.scilifelab.se/researcher/b85588d272854ff2a9d6c4e364529971.json"}}], "type": "journal article", "published": "2020-12-00", "journal": {"title": "J. Pathol.", "issn": "1096-9896", "issn-l": "0022-3417", "volume": "252", "issue": "4", "pages": "384-397"}, "abstract": "Clear cell renal cell carcinoma (ccRCC) is the most common form of renal cancer. Due to inactivation of the von Hippel-Lindau tumour suppressor, the hypoxia-inducible transcription factors (HIFs) are constitutively activated in these tumours, resulting in a pseudo-hypoxic phenotype. The HIFs induce the expression of genes involved in angiogenesis and cell survival, but they also reset the cellular metabolism to protect cells from oxygen and nutrient deprivation. ccRCC tumours are highly vascularized and the cytoplasm of the cancer cells is filled with lipid droplets and glycogen, resulting in the histologically distinctive pale (clear) cytoplasm. Intratumoural heterogeneity may occur, and in some tumours, areas with granular, eosinophilic cytoplasm are found. Little is known regarding these traits and how they relate to the coexistent clear cell component, yet eosinophilic ccRCC is associated with higher grade and clinically more aggressive tumours. In this study, we have for the first time performed RNA sequencing comparing histologically verified clear cell and eosinophilic areas from ccRCC tissue, aiming to analyse the characteristics of these cell types. Findings from RNA sequencing were confirmed by immunohistochemical staining of biphasic ccRCC. We found that the eosinophilic phenotype displayed a higher proliferative drive and lower differentiation, and we confirmed a correlation to tumours of higher stage. We further identified mutations of the tumour suppressor p53 (TP53) exclusively in the eosinophilic ccRCC component, where mTORC1 activity was also elevated. Also, eosinophilic areas were less vascularized, yet harboured more abundant infiltrating immune cells. The cytoplasm of clear cell ccRCC cells was filled with lipids but had very low mitochondrial content, while the reverse was found in eosinophilic tissue. We herein suggest possible transcriptional mechanisms behind these phenomena. \u00a9 2020 The Authors. The Journal of Pathology published by John Wiley & Sons, Ltd. on behalf of The Pathological Society of Great Britain and Ireland.", "doi": "10.1002/path.5532", "pmid": "32815150", "labels": {"NGI Stockholm (Genomics Production)": "Service", "National Genomics Infrastructure": "Service", "NGI Stockholm (Genomics Applications)": "Service", "Bioinformatics Support for Computational Resources": "Service"}, "xrefs": [{"db": "pmc", "key": "PMC7756750"}], "notes": [], "created": "2020-12-07T16:32:32.781Z", "modified": "2024-01-16T13:48:41.254Z"}]}