Microarray profiling of hypothalamic gene expression changes in Huntington's disease mouse models

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Dickson, ElnaLund University,Lunds universitet,Institutionen för experimentell medicinsk vetenskap,Medicinska fakulteten,Biomarkörer vid hjärnsjukdomar,Forskargrupper vid Lunds universitet,Department of Experimental Medical Science,Faculty of Medicine,Biomarkers in Brain Disease,Lund University Research Groups (author)

Microarray profiling of hypothalamic gene expression changes in Huntington's disease mouse models

Article/chapterEnglish2022

Publisher, publication year, extent ...

2022-11-03
Frontiers Media SA,2022
16 s.

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LIBRIS-ID:oai:lup.lub.lu.se:d0c9fb40-1972-470f-a135-b6234294c04b
https://lup.lub.lu.se/record/d0c9fb40-1972-470f-a135-b6234294c04bURI
https://doi.org/10.3389/fnins.2022.1027269DOI

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Language:English
Summary in:English

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Subject category:art swepub-publicationtype
Subject category:ref swepub-contenttype

Notes

Structural changes and neuropathology in the hypothalamus have been suggested to contribute to the non-motor manifestations of Huntington's disease (HD), a neurodegenerative disorder caused by an expanded cytosine-adenine-guanine (CAG) repeat in the huntingtin (HTT) gene. In this study, we investigated whether hypothalamic HTT expression causes transcriptional changes. Hypothalamic RNA was isolated from two different HD mouse models and their littermate controls; BACHD mice with ubiquitous expression of full-length mutant HTT (mHTT) and wild-type mice with targeted hypothalamic overexpression of either wild-type HTT (wtHTT) or mHTT fragments. The mHTT and wtHTT groups showed the highest number of differentially expressed genes compared to the BACHD mouse model. Gene Set Enrichment Analysis (GSEA) with leading-edge analysis showed that suppressed sterol- and cholesterol metabolism were shared between hypothalamic wtHTT and mHTT overexpression. Most distinctive for mHTT overexpression was the suppression of neuroendocrine networks, in which qRT-PCR validation confirmed significant downregulation of neuropeptides with roles in feeding behavior; hypocretin neuropeptide precursor (Hcrt), tachykinin receptor 3 (Tacr3), cocaine and amphetamine-regulated transcript (Cart) and catecholamine-related biological processes; dopa decarboxylase (Ddc), histidine decarboxylase (Hdc), tyrosine hydroxylase (Th), and vasoactive intestinal peptide (Vip). In BACHD mice, few hypothalamic genes were differentially expressed compared to age-matched WT controls. However, GSEA indicated an enrichment of inflammatory- and gonadotropin-related processes at 10 months. In conclusion, we show that both wtHTT and mHTT overexpression change hypothalamic transcriptome profile, specifically mHTT, altering neuroendocrine circuits. In contrast, the ubiquitous expression of full-length mHTT in the BACHD hypothalamus moderately affects the transcriptomic profile.

Subject headings and genre

MEDICIN OCH HÄLSOVETENSKAP Medicinska och farmaceutiska grundvetenskaper Neurovetenskaper hsv//swe
MEDICAL AND HEALTH SCIENCES Basic Medicine Neurosciences hsv//eng
MEDICIN OCH HÄLSOVETENSKAP Medicinska och farmaceutiska grundvetenskaper Cell- och molekylärbiologi hsv//swe
MEDICAL AND HEALTH SCIENCES Basic Medicine Cell and Molecular Biology hsv//eng
Huntington’s disease
neuroendocrine
hypothalamus
microarray
HD mouse models
huntingtin
differential expression

Added entries (persons, corporate bodies, meetings, titles ...)

Dwijesha, Amoolya SaiLund University,Lunds universitet,Institutionen för experimentell medicinsk vetenskap,Medicinska fakulteten,Translationell neuroendokrinologi,Forskargrupper vid Lunds universitet,Department of Experimental Medical Science,Faculty of Medicine,Translational Neuroendocrinology,Lund University Research Groups(Swepub:lu)am6302sa (author)
Andersson, NatalieLund University,Lunds universitet,Avdelningen för klinisk genetik,Institutionen för laboratoriemedicin,Medicinska fakulteten,Cancercellers evolution,Forskargrupper vid Lunds universitet,Division of Clinical Genetics,Department of Laboratory Medicine,Faculty of Medicine,Pathways of cancer cell evolution,Lund University Research Groups(Swepub:lu)na8883an (author)
Lundh, SofiaLund University,Lunds universitet,Institutionen för experimentell medicinsk vetenskap,Medicinska fakulteten,Translationell neuroendokrinologi,Forskargrupper vid Lunds universitet,Department of Experimental Medical Science,Faculty of Medicine,Translational Neuroendocrinology,Lund University Research Groups(Swepub:lu)so3600hu (author)
Björkqvist, MariaLund University,Lunds universitet,Institutionen för experimentell medicinsk vetenskap,Medicinska fakulteten,Biomarkörer vid hjärnsjukdomar,Forskargrupper vid Lunds universitet,Department of Experimental Medical Science,Faculty of Medicine,Biomarkers in Brain Disease,Lund University Research Groups(Swepub:lu)eken-mab (author)
Petersén, ÅsaLund University,Lunds universitet,Institutionen för experimentell medicinsk vetenskap,Medicinska fakulteten,Translationell neuroendokrinologi,Forskargrupper vid Lunds universitet,Department of Experimental Medical Science,Faculty of Medicine,Translational Neuroendocrinology,Lund University Research Groups(Swepub:lu)mphy-apn (author)
Soylu-Kucharz, RanaLund University,Lunds universitet,Institutionen för experimentell medicinsk vetenskap,Medicinska fakulteten,Biomarkörer vid hjärnsjukdomar,Forskargrupper vid Lunds universitet,Department of Experimental Medical Science,Faculty of Medicine,Biomarkers in Brain Disease,Lund University Research Groups(Swepub:lu)med-rso (author)
Institutionen för experimentell medicinsk vetenskapMedicinska fakulteten (creator_code:org_t)

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