{"entity": "researcher", "timestamp": "2026-07-11T23:23:15.170Z", "family": "Zhou", "given": "Kai", "initials": "K", "orcid": "0000-0003-1026-757X", "affiliations": ["Henan Neurodevelopment Engineering Research Center for Children, Children's Hospital Affiliated to Zhengzhou University, Zhengzhou, China. kai.zhou@ki.se.", "Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden. kai.zhou@ki.se."], "links": {"self": {"href": "https://publications.scilifelab.se/researcher/435dbc44e7fd468a9f2284cbe8810d52.json"}, "display": {"href": "https://publications.scilifelab.se/researcher/435dbc44e7fd468a9f2284cbe8810d52"}}, "publications": [{"entity": "publication", "iuid": "244765187cff4949831aab7eacfe9384", "links": {"self": {"href": "https://publications.scilifelab.se/publication/244765187cff4949831aab7eacfe9384.json"}, "display": {"href": "https://publications.scilifelab.se/publication/244765187cff4949831aab7eacfe9384"}}, "title": "An overlooked subset of Cx3cr1wt/wt microglia in the Cx3cr1CreER-Eyfp/wt mouse has a repopulation advantage over Cx3cr1CreER-Eyfp/wt microglia following microglial depletion", "authors": [{"family": "Zhou", "given": "Kai", "initials": "K", "orcid": "0000-0003-1026-757X", "researcher": {"href": "https://publications.scilifelab.se/researcher/435dbc44e7fd468a9f2284cbe8810d52.json"}}, {"family": "Han", "given": "Jinming", "initials": "J"}, {"family": "Lund", "given": "Harald", "initials": "H"}, {"family": "Boggavarapu", "given": "Nageswara Rao", "initials": "NR"}, {"family": "Lauschke", "given": "Volker M", "initials": "VM"}, {"family": "Goto", "given": "Shinobu", "initials": "S"}, {"family": "Cheng", "given": "Huaitao", "initials": "H"}, {"family": "Wang", "given": "Yuyu", "initials": "Y"}, {"family": "Tachi", "given": "Asuka", "initials": "A"}, {"family": "Xie", "given": "Cuicui", "initials": "C"}, {"family": "Zhu", "given": "Keying", "initials": "K"}, {"family": "Sun", "given": "Ying", "initials": "Y"}, {"family": "Osman", "given": "Ahmed M", "initials": "AM"}, {"family": "Liang", "given": "Dong", "initials": "D"}, {"family": "Han", "given": "Wei", "initials": "W"}, {"family": "Gemzell-Danielsson", "given": "Kristina", "initials": "K"}, {"family": "Betsholtz", "given": "Christer", "initials": "C"}, {"family": "Zhang", "given": "Xing Mei", "initials": "XM"}, {"family": "Zhu", "given": "Changlian", "initials": "C"}, {"family": "Enge", "given": "Martin", "initials": "M"}, {"family": "Joseph", "given": "Bertrand", "initials": "B"}, {"family": "Harris", "given": "Robert A", "initials": "RA"}, {"family": "Blomgren", "given": "Klas", "initials": "K", "orcid": "0000-0002-0476-7271", "researcher": {"href": "https://publications.scilifelab.se/researcher/2fb3b554177d481ebc9d4aa0f3b1fbc4.json"}}], "type": "journal-article", "published": "2022-12-00", "journal": {"title": "J Neuroinflammation", "issn": "1742-2094", "issn-l": "1742-2094", "volume": "19", "issue": "1", "pages": "20"}, "abstract": "Fluorescent reporter labeling and promoter-driven Cre-recombinant technologies have facilitated cellular investigations of physiological and pathological processes, including the widespread use of the Cx3cr1CreER-Eyfp/wt mouse strain for studies of microglia.\r\n\r\nImmunohistochemistry, Flow Cytometry, RNA sequencing and whole-genome sequencing were used to identify the subpopulation of microglia in Cx3cr1CreER-Eyfp/wt mouse brains. Genetically mediated microglia depletion using Cx3cr1CreER-Eyfp/wtRosa26DTA/wt mice and CSF1 receptor inhibitor PLX3397 were used to deplete microglia. Primary microglia proliferation and migration assay were used for in vitro studies.\r\n\r\nWe unexpectedly identified a subpopulation of microglia devoid of genetic modification, exhibiting higher Cx3cr1 and CX3CR1 expression than Cx3cr1CreER-Eyfp/wtCre+Eyfp+ microglia in Cx3cr1CreER-Eyfp/wt mouse brains, thus termed Cx3cr1highCre-Eyfp- microglia. This subpopulation constituted less than 1% of all microglia under homeostatic conditions, but after Cre-driven DTA-mediated microglial depletion, Cx3cr1highCre-Eyfp- microglia escaped depletion and proliferated extensively, eventually occupying one-third of the total microglial pool. We further demonstrated that the Cx3cr1highCre-Eyfp- microglia had lost their genetic heterozygosity and become homozygous for wild-type Cx3cr1. Therefore, Cx3cr1highCre-Eyfp- microglia are Cx3cr1wt/wtCre-Eyfp-. Finally, we demonstrated that CX3CL1-CX3CR1 signaling regulates microglial repopulation both in vivo and in vitro.\r\n\r\nOur results raise a cautionary note regarding the use of Cx3cr1CreER-Eyfp/wt mouse strains, particularly when interpreting the results of fate mapping, and microglial depletion and repopulation studies.", "doi": "10.1186/s12974-022-02381-6", "pmid": "35062962", "labels": {"Eukaryotic Single Cell Genomics (ESCG)": "Service", "NGI Stockholm (Genomics Production)": "Service", "NGI Stockholm (Genomics Applications)": "Service", "NGI Single cell": "Service", "National Genomics Infrastructure": "Service"}, "xrefs": [{"db": "pmc", "key": "PMC8783445"}, {"db": "pii", "key": "10.1186/s12974-022-02381-6"}], "notes": [], "created": "2022-12-01T13:48:40.480Z", "modified": "2024-02-12T08:44:32.493Z"}]}