GV1001 Inhibits the Severity of the Ligature-Induced Periodontitis and the Vascular Lipid Deposition Associated with the Periodontitis in Mice

GV1001, a 16 amino acid peptide derived from the catalytic segment of human telomerase reverse transcriptase, was developed as an anti-cancer vaccine. Subsequently, it was found to exhibit anti-inflammatory and anti-Alzheimer's disease properties. Periodontitis is a risk factor for a variety of...

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Bibliographic Details
Published in:	International journal of molecular sciences Vol. 24; no. 16; p. 12566
Main Authors:	Kim, Sharon Y, Kim, Yun-Jeong, Kim, Suyang, Momeni, Mersedeh, Lee, Alicia, Treanor, Alexandra, Kim, Sangjae, Kim, Reuben H, Park, No-Hee
Format:	Journal Article
Language:	English
Published:	Switzerland MDPI AG 01-08-2023 MDPI
Subjects:	Alzheimer's disease Animals Apolipoproteins Arteries Atherosclerosis Cancer Vaccines Cardiovascular disease Cytokines Disease prevention Endothelial Cells Gum disease GV1001 Humans Inflammation Ischemia Lipids Mice Periodontitis Risk factors Scientific equipment and supplies industry systemic and vascular inflammation Tumor necrosis factor-TNF Vaccines Vaccines, Subunit United Kingdom California United States Massachusetts Japan Missouri atherosclerosis systemic and vascular inflammation GV1001 periodontitis
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Summary:	GV1001, a 16 amino acid peptide derived from the catalytic segment of human telomerase reverse transcriptase, was developed as an anti-cancer vaccine. Subsequently, it was found to exhibit anti-inflammatory and anti-Alzheimer's disease properties. Periodontitis is a risk factor for a variety of systemic diseases, including atherosclerosis, a process in which chronic systemic and vascular inflammation results in the formation of plaques containing lipids, macrophages, foam cells, and tissue debris on the vascular intima. Thus, we investigated the effect of GV1001 on the severity of ligature-induced periodontitis, vascular inflammation, and arterial lipid deposition in mice. GV1001 notably reduced the severity of ligature-induced periodontitis by inhibiting gingival and systemic inflammation, alveolar bone loss, and vascular inflammation in wild-type mice. It also significantly lowered the amount of lipid deposition in the arterial wall in -deficient mice receiving ligature placement without changing the serum lipid profile. In vitro, we found that GV1001 inhibited the Receptor Activator of NF-κB ligand (RANKL)-induced osteoclast formation and tumor necrosis factor-α (TNF-α)-induced phenotypic changes in endothelial cells. In conclusion, our study suggests that GV1001 prevents the exacerbation of periodontitis and atherosclerosis associated with periodontitis partly by inhibiting local, systemic, and vascular inflammation and phenotypic changes of vascular endothelial cells.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors contributed equally to this work. Present address: Marist School, 3790 Ashford Dunwoody Rd, NE, Atlanta, GA 30319, USA.
ISSN:	1422-0067 1661-6596 1422-0067
DOI:	10.3390/ijms241612566