{"entity": "researcher", "timestamp": "2026-07-12T18:10:27.985Z", "family": "Nair", "given": "Syam", "initials": "S", "orcid": "0000-0001-8470-2162", "affiliations": ["Centre of Perinatal Medicine and Health, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.", "Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden."], "links": {"self": {"href": "https://publications.scilifelab.se/researcher/733eacd288ce4eefaad48c391436a319.json"}, "display": {"href": "https://publications.scilifelab.se/researcher/733eacd288ce4eefaad48c391436a319"}}, "publications": [{"entity": "publication", "iuid": "237d4257446a41e89c2141735913e512", "links": {"self": {"href": "https://publications.scilifelab.se/publication/237d4257446a41e89c2141735913e512.json"}, "display": {"href": "https://publications.scilifelab.se/publication/237d4257446a41e89c2141735913e512"}}, "title": "Induction of Mitochondrial Fragmentation and Mitophagy after Neonatal Hypoxia-Ischemia.", "authors": [{"family": "Nair", "given": "Syam", "initials": "S", "orcid": "0000-0001-8470-2162", "researcher": {"href": "https://publications.scilifelab.se/researcher/733eacd288ce4eefaad48c391436a319.json"}}, {"family": "Leverin", "given": "Anna-Lena", "initials": "AL"}, {"family": "Rocha-Ferreira", "given": "Eridan", "initials": "E", "orcid": "0000-0002-9342-4691", "researcher": {"href": "https://publications.scilifelab.se/researcher/9c297cd7e1a3447aa61e5faddcb90693.json"}}, {"family": "Sobotka", "given": "Kristina S", "initials": "KS"}, {"family": "Thornton", "given": "Claire", "initials": "C", "orcid": "0000-0001-7676-3272", "researcher": {"href": "https://publications.scilifelab.se/researcher/80dc80b67a7c4b949318e1f5aa2666f9.json"}}, {"family": "Mallard", "given": "Carina", "initials": "C", "orcid": "0000-0001-8953-919X", "researcher": {"href": "https://publications.scilifelab.se/researcher/2d0fa7de10554b5bb5a0e1ee64902aa1.json"}}, {"family": "Hagberg", "given": "Henrik", "initials": "H"}], "type": "journal article", "published": "2022-04-01", "journal": {"title": "Cells", "issn": "2073-4409", "volume": "11", "issue": "7", "issn-l": "2073-4409"}, "abstract": "Hypoxia-ischemia (HI) leads to immature brain injury mediated by mitochondrial stress. If damaged mitochondria cannot be repaired, mitochondrial permeabilization ensues, leading to cell death. Non-optimal turnover of mitochondria is critical as it affects short and long term structural and functional recovery and brain development. Therefore, disposal of deficient mitochondria via mitophagy and their replacement through biogenesis is needed. We utilized mt-Keima reporter mice to quantify mitochondrial morphology (fission, fusion) and mitophagy and their mechanisms in primary neurons after Oxygen Glucose Deprivation (OGD) and in brain sections after neonatal HI. Molecular mechanisms of PARK2-dependent and -independent pathways of mitophagy were investigated in vivo by PCR and Western blotting. Mitochondrial morphology and mitophagy were investigated using live cell microscopy. In primary neurons, we found a primary fission wave immediately after OGD with a significant increase in mitophagy followed by a secondary phase of fission at 24 h following recovery. Following HI, mitophagy was upregulated immediately after HI followed by a second wave at 7 days. Western blotting suggests that both PINK1/Parkin-dependent and -independent mechanisms, including NIX and FUNDC1, were upregulated immediately after HI, whereas a PINK1/Parkin mechanism predominated 7 days after HI. We hypothesize that excessive mitophagy in the early phase is a pathologic response which may contribute to secondary energy depletion, whereas secondary mitophagy may be involved in post-HI regeneration and repair.", "doi": "10.3390/cells11071193", "pmid": "35406757", "labels": {"Integrated Microscopy Technologies Gothenburg": "Service"}, "xrefs": [{"db": "pmc", "key": "PMC8997592"}, {"db": "pii", "key": "cells11071193"}], "notes": [], "created": "2023-02-16T08:24:58.046Z", "modified": "2023-02-16T08:24:58.149Z"}, {"entity": "publication", "iuid": "200f9749c28742c2bd9c1629be8a4eb0", "links": {"self": {"href": "https://publications.scilifelab.se/publication/200f9749c28742c2bd9c1629be8a4eb0.json"}, "display": {"href": "https://publications.scilifelab.se/publication/200f9749c28742c2bd9c1629be8a4eb0"}}, "title": "Lipopolysaccharide-induced alteration of mitochondrial morphology induces a metabolic shift in microglia modulating the inflammatory response in vitro and in vivo.", "authors": [{"family": "Nair", "given": "Syam", "initials": "S", "orcid": "0000-0001-8470-2162", "researcher": {"href": "https://publications.scilifelab.se/researcher/733eacd288ce4eefaad48c391436a319.json"}}, {"family": "Sobotka", "given": "Kristina S", "initials": "KS"}, {"family": "Joshi", "given": "Pooja", "initials": "P"}, {"family": "Gressens", "given": "Pierre", "initials": "P"}, {"family": "Fleiss", "given": "Bobbi", "initials": "B"}, {"family": "Thornton", "given": "Claire", "initials": "C"}, {"family": "Mallard", "given": "Carina", "initials": "C"}, {"family": "Hagberg", "given": "Henrik", "initials": "H"}], "type": "journal article", "published": "2019-06-00", "journal": {"title": "Glia", "issn": "1098-1136", "volume": "67", "issue": "6", "pages": "1047-1061", "issn-l": "0894-1491"}, "abstract": "Accumulating evidence suggests that changes in the metabolic signature of microglia underlie their response to inflammation. We sought to increase our knowledge of how pro-inflammatory stimuli induce metabolic changes. Primary microglia exposed to lipopolysaccharide (LPS)-expressed excessive fission leading to more fragmented mitochondria than tubular mitochondria. LPS-mediated Toll-like receptor 4 (TLR4) activation also resulted in metabolic reprogramming from oxidative phosphorylation to glycolysis. Blockade of mitochondrial fission by Mdivi-1, a putative mitochondrial division inhibitor led to the reversal of the metabolic shift. Mdivi-1 treatment also normalized the changes caused by LPS exposure, namely an increase in mitochondrial reactive oxygen species production and mitochondrial membrane potential as well as accumulation of key metabolic intermediate of TCA cycle succinate. Moreover, Mdivi-1 treatment substantially reduced LPS induced cytokine and chemokine production. Finally, we showed that Mdivi-1 treatment attenuated expression of genes related to cytotoxic, repair, and immunomodulatory microglia phenotypes in an in vivo neuroinflammation paradigm. Collectively, our data show that the activation of microglia to a classically pro-inflammatory state is associated with a switch to glycolysis that is mediated by mitochondrial fission, a process which may be a pharmacological target for immunomodulation.", "doi": "10.1002/glia.23587", "pmid": "30637805", "labels": {"Integrated Microscopy Technologies Gothenburg": "Service"}, "xrefs": [], "notes": [], "created": "2020-01-23T16:10:15.580Z", "modified": "2021-06-21T11:52:41.828Z"}]}