{"entity": "researcher", "timestamp": "2026-04-20T22:25:08.610Z", "family": "Mallard", "given": "Carina", "initials": "C", "orcid": "0000-0001-8953-919X", "affiliations": [], "links": {"self": {"href": "https://publications.scilifelab.se/researcher/2d0fa7de10554b5bb5a0e1ee64902aa1.json"}, "display": {"href": "https://publications.scilifelab.se/researcher/2d0fa7de10554b5bb5a0e1ee64902aa1"}}, "publications": [{"entity": "publication", "iuid": "76a1e6398a4d4115b774554b4b61f807", "links": {"self": {"href": "https://publications.scilifelab.se/publication/76a1e6398a4d4115b774554b4b61f807.json"}, "display": {"href": "https://publications.scilifelab.se/publication/76a1e6398a4d4115b774554b4b61f807"}}, "title": "Transcriptome network analysis links perinatal Staphylococcus epidermidis infection to microglia reprogramming in the immature hippocampus.", "authors": [{"family": "Gravina", "given": "Giacomo", "initials": "G"}, {"family": "Ardalan", "given": "Maryam", "initials": "M"}, {"family": "Chumak", "given": "Tetyana", "initials": "T"}, {"family": "Rydbeck", "given": "Halfdan", "initials": "H"}, {"family": "Wang", "given": "Xiaoyang", "initials": "X", "orcid": "0000-0001-9717-8160", "researcher": {"href": "https://publications.scilifelab.se/researcher/70fbed19bca84bec93f558168444227a.json"}}, {"family": "Ek", "given": "Carl Joakim", "initials": "CJ"}, {"family": "Mallard", "given": "Carina", "initials": "C", "orcid": "0000-0001-8953-919X", "researcher": {"href": "https://publications.scilifelab.se/researcher/2d0fa7de10554b5bb5a0e1ee64902aa1.json"}}], "type": "journal article", "published": "2023-09-00", "journal": {"title": "Glia", "issn": "1098-1136", "volume": "71", "issue": "9", "pages": "2234-2249", "issn-l": "0894-1491"}, "abstract": "Staphylococcus epidermidis (S. epidermidis) is the most common nosocomial pathogen in preterm infants and associated with increased risk of cognitive delay, however, underlying mechanisms are unknown. We employed morphological, transcriptomic and physiological methods to extensively characterize microglia in the immature hippocampus following S. epidermidis infection. 3D morphological analysis revealed activation of microglia after S. epidermidis. Differential expression combined with network analysis identified NOD-receptor signaling and trans-endothelial leukocyte trafficking as major mechanisms in microglia. In support, active caspase-1 was increased in the hippocampus and using the LysM-eGFP knock-in transgenic mouse, we demonstrate infiltration of leukocytes to the brain together with disruption of the blood-brain barrier. Our findings identify activation of microglia inflammasome as a major mechanism underlying neuroinflammation following infection. The results demonstrate that neonatal S. epidermidis infection share analogies with S. aureus and neurological diseases, suggesting a previously unrecognized important role in neurodevelopmental disorders in preterm born children.", "doi": "10.1002/glia.24389", "pmid": "37246946", "labels": {"Clinical Genomics Gothenburg": "Service", "Clinical Genomics": "Service"}, "xrefs": [], "notes": [], "created": "2023-11-30T22:32:41.569Z", "modified": "2023-11-30T22:32:41.607Z"}, {"entity": "publication", "iuid": "ac80952db59f49f3b1c15eec06392e65", "links": {"self": {"href": "https://publications.scilifelab.se/publication/ac80952db59f49f3b1c15eec06392e65.json"}, "display": {"href": "https://publications.scilifelab.se/publication/ac80952db59f49f3b1c15eec06392e65"}}, "title": "Two different isoforms of osteopontin modulate myelination and axonal integrity.", "authors": [{"family": "Nilsson", "given": "Gisela", "initials": "G", "orcid": "0000-0003-4423-5082", "researcher": {"href": "https://publications.scilifelab.se/researcher/c07681f5131b4c58bd71119c56f5d435.json"}}, {"family": "Mottahedin", "given": "Amin", "initials": "A", "orcid": "0000-0002-3677-2198", "researcher": {"href": "https://publications.scilifelab.se/researcher/82a4c6f53ae241edaf5147addb082567.json"}}, {"family": "Zelco", "given": "Aura", "initials": "A", "orcid": "0000-0002-5851-6355", "researcher": {"href": "https://publications.scilifelab.se/researcher/f66e84b556ab4454b96ba929cfa2b104.json"}}, {"family": "Lauschke", "given": "Volker M", "initials": "VM", "orcid": "0000-0002-1140-6204", "researcher": {"href": "https://publications.scilifelab.se/researcher/29c123916fbf4948a911560c1a259496.json"}}, {"family": "Ek", "given": "C Joakim", "initials": "CJ", "orcid": "0000-0002-5764-7679", "researcher": {"href": "https://publications.scilifelab.se/researcher/991c705e88dd472cae9e98ad540660ab.json"}}, {"family": "Song", "given": "Juan", "initials": "J"}, {"family": "Ardalan", "given": "Maryam", "initials": "M", "orcid": "0000-0003-3414-1584", "researcher": {"href": "https://publications.scilifelab.se/researcher/ceef7775ba414a1ab0f5039db2f0014b.json"}}, {"family": "Hua", "given": "Sha", "initials": "S"}, {"family": "Zhang", "given": "Xiaoli", "initials": "X", "orcid": "0000-0001-5111-9405", "researcher": {"href": "https://publications.scilifelab.se/researcher/3d5f1af1b5f3452d8db56bbe3eea440c.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", "orcid": "0000-0003-3962-1448", "researcher": {"href": "https://publications.scilifelab.se/researcher/ca1150b5f07c441096f2716c0564e1d0.json"}}, {"family": "Leavenworth", "given": "Jianmei W", "initials": "JW", "orcid": "0000-0002-4100-9883", "researcher": {"href": "https://publications.scilifelab.se/researcher/d1b287368adf4edabe671e33ab56c550.json"}}, {"family": "Wang", "given": "Xiaoyang", "initials": "X", "orcid": "0000-0001-9717-8160", "researcher": {"href": "https://publications.scilifelab.se/researcher/70fbed19bca84bec93f558168444227a.json"}}], "type": "journal article", "published": "2023-08-00", "journal": {"title": "FASEB Bioadv", "issn": "2573-9832", "issn-l": null, "volume": "5", "issue": "8", "pages": "336-353"}, "abstract": "Abnormal myelination underlies the pathology of white matter diseases such as preterm white matter injury and multiple sclerosis. Osteopontin (OPN) has been suggested to play a role in myelination. Murine OPN mRNA is translated into a secreted isoform (sOPN) or an intracellular isoform (iOPN). Whether there is an isoform-specific involvement of OPN in myelination is unknown. Here we generated mouse models that either lacked both OPN isoforms in all cells (OPN-KO) or lacked sOPN systemically but expressed iOPN specifically in oligodendrocytes (OLs-iOPN-KI). Transcriptome analysis of isolated oligodendrocytes from the neonatal brain showed that genes and pathways related to increase of myelination and altered cell cycle control were enriched in the absence of the two OPN isoforms in OPN-KO mice compared to control mice. Accordingly, adult OPN-KO mice showed an increased axonal myelination, as revealed by transmission electron microscopy imaging, and increased expression of myelin-related proteins. In contrast, neonatal oligodendrocytes from OLs-iOPN-KI mice compared to control mice showed differential regulation of genes and pathways related to the increase of cell adhesion, motility, and vasculature development, and the decrease of axonal/neuronal development. OLs-iOPN-KI mice showed abnormal myelin formation in the early phase of myelination in young mice and signs of axonal degeneration in adulthood. These results suggest an OPN isoform-specific involvement, and a possible interplay between the isoforms, in myelination, and axonal integrity. Thus, the two isoforms of OPN need to be separately considered in therapeutic strategies targeting OPN in white matter injury and diseases.", "doi": "10.1096/fba.2023-00030", "pmid": "37554545", "labels": {"Clinical Genomics Gothenburg": "Service", "Integrated Microscopy Technologies Gothenburg": "Service", "Clinical Genomics": "Service"}, "xrefs": [{"db": "pmc", "key": "PMC10405251"}, {"db": "pii", "key": "FBA21405"}], "notes": [], "created": "2023-11-30T22:35:19.238Z", "modified": "2023-12-03T13:28:50.770Z"}, {"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": "982044cf67514ddeb9751b625529811b", "links": {"self": {"href": "https://publications.scilifelab.se/publication/982044cf67514ddeb9751b625529811b.json"}, "display": {"href": "https://publications.scilifelab.se/publication/982044cf67514ddeb9751b625529811b"}}, "title": "Intranasal C3a treatment ameliorates cognitive impairment in a mouse model of neonatal hypoxic-ischemic brain injury.", "authors": [{"family": "Mor\u00e1n", "given": "Javier", "initials": "J"}, {"family": "Stokowska", "given": "Anna", "initials": "A", "orcid": "0000-0001-5237-3341", "researcher": {"href": "https://publications.scilifelab.se/researcher/ba5e258c6d934db08ed52a70cf6da7b9.json"}}, {"family": "Walker", "given": "Frederik R", "initials": "FR"}, {"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"}, {"family": "Pekna", "given": "Marcela", "initials": "M", "orcid": "0000-0003-2734-8237", "researcher": {"href": "https://publications.scilifelab.se/researcher/cf0f51a8f05b4e659ba192642603a7d6.json"}}], "type": "journal article", "published": "2017-04-00", "journal": {"title": "Exp. Neurol.", "issn": "1090-2430", "volume": "290", "issue": null, "pages": "74-84", "issn-l": "0014-4886"}, "abstract": "Perinatal asphyxia-induced brain injury is often associated with irreversible neurological complications such as intellectual disability and cerebral palsy but available therapies are limited. Novel neuroprotective therapies as well as approaches stimulating neural plasticity mechanism that can compensate for cell death after hypoxia-ischemia (HI) are urgently needed. We previously reported that single i.c.v. injection of complement-derived peptide C3a 1h after HI induction prevented HI-induced cognitive impairment when mice were tested as adults. Here, we tested the effects of intranasal treatment with C3a on HI-induced cognitive deficit. Using the object recognition test, we found that intranasal C3a treated mice were protected from HI-induced impairment of memory function assessed 6weeks after HI induction. C3a treatment ameliorated HI-induced reactive gliosis in the hippocampus, while it did not affect the extent of hippocampal tissue loss, neuronal cell density, expression of the pan-synaptic marker synapsin I or the expression of growth associated protein 43. In conclusion, our results reveal that brief pharmacological treatment with C3a using a clinically feasible non-invasive mode of administration ameliorates HI-induced cognitive impairment. Intranasal administration is a plausible route to deliver C3a into the brain of asphyxiated infants at high risk of developing hypoxic-ischemic encephalopathy.", "doi": "10.1016/j.expneurol.2017.01.001", "pmid": "28062175", "labels": {"Integrated Microscopy Technologies Gothenburg": "Service"}, "xrefs": [{"db": "pii", "key": "S0014-4886(17)30001-8"}], "notes": [], "created": "2020-01-23T16:35:48.152Z", "modified": "2021-06-21T15:40:51.853Z"}]}