ArticleJournal of veterinary internal medicine2019
Association of sustained supraphysiologic hyperinsulinemia and inflammatory signaling within the digital lamellae in light-breed horses.
Article in Journal of veterinary internal medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- Interleukins decrease epithelial protein and gene expression by K14 + CD105+ equine hoof progenitor cells.Stem cell research & therapy · 2026Article
- Quercetin alleviates LPS-induced inflammatory response in dairy cow lamellar keratinocytes through PI3K/Akt/NF-κB signaling pathway.BMC veterinary research · 2026Article
- Digital lamellar inflammatory signaling in an experimental model of equine preferential weight bearing.Journal of veterinary internal medicine · 2023Article
- Conditioned serum in vitro treatment of chondrocyte pellets and osteoarthritic explants.Equine veterinary journal · 2023Article
- Effect of digital hypothermia on lamellar inflammatory signaling in the euglycemic hyperinsulinemic clamp laminitis model.Journal of veterinary internal medicine · 2020Article
- Interleukin-17A pathway target genes are upregulated in Equus caballus supporting limb laminitis.PloS one · 2020Article
- Association of sustained supraphysiologic hyperinsulinemia and inflammatory signaling within the digital lamellae in light-breed horses.Journal of veterinary internal medicine · 2019Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundHyperinsulinemia is associated with equine laminitis, and digital lamellar inflammation in equine metabolic syndrome-associated laminitis (EMSAL) is modest when compared with sepsis-associated laminitis.
objectivesTo characterize digital lamellar inflammation in horses in a euglycemic-hyperinsulinemic clamp (EHC) model of laminitis. ANIMALS: Sixteen healthy adult Standardbred horses.
methodsProspective experimental study. Horses underwent EHC or saline infusion (CON) for 48 hours or until the onset of Obel grade 1 laminitis. Horses were euthanized, and digital lamellar tissue was collected and analyzed via polymerase chain reaction (pro-inflammatory cytokine and chemokine genes-CXCL1, CXCL6, CXCL8, IL-6, MCP-1, MCP-2, IL-1β, IL11, cyclooxygenases 1 and 2, tumor necrosis factor alpha [TNF-α], E-selectin, and ICAM-1), immunoblotting (phosphorylated and total signal transducer and activator of transcription 1 [STAT1], STAT3, and p38MAPK), and immunohistochemistry (markers of leukocyte infiltration: CD163, MAC387).
resultsLamellar mRNA concentrations of IL-1β, IL-6, IL-11, COX-2, and E-selectin were increased; the concentration of COX-1 was decreased; and concentrations of CXCL1, CXCL6, MCP-1, MCP-2, IL-8, TNF-α and ICAM-1 were not significantly different in the EHC group compared to the CON group (P ≤ .003). Lamellar concentrations of phosphorylated STAT proteins (P-STAT1 [S727], P-STAT1 [Y701], P-STAT3 [S727], and P-STAT3 [Y705]) were increased in the EHC group compared to the CON group, with phosphorylated STAT3 localizing to nuclei of lamellar basal epithelial cells. There was no change in the lamellar concentration of P-p38 MAPK (T180/Y182), but the concentration of total p38 MAPK was decreased in the EHC samples. There was no evidence of notable lamellar leukocyte emigration. CONCLUSIONS AND CLINICAL IMPORTANCE: These results establish a role for lamellar inflammatory signaling under conditions associated with EMSAL.
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