The expression of luteinizing hormone (LH) receptors has been reported in canine nonneoplastic and neoplastic lymphocytes. This study aimed to determine the effect of LH receptor activation in neoplastic canine T lymphocytes. Cell lines (CLC, CLK, EMA) derived from 3 dogs with primary T-cell lymphoma were used. Cell lines were previously phenotyped and evaluated for LH receptor expression with flow cytometry. Cell lines were stimulated with increasing concentrations (0, 4, 400, and 4,000 U/mL) of human chorionic gonadotropin (hCG; an LH receptor agonist), RNA was extracted, cDNA was synthesized, and gene expression was determined using quantitative PCR and the 2-ΔΔCt method. Cell lines were stimulated with the same increasing concentrations of hCG, and cell proliferation, adhesion, and transmigration were determined using commercial assays. The effects of LH receptor activation were compared between hCG concentrations using a one-way ANOVA. Significance was defined as P < .05. LH receptor stimulation increased LH receptor gene expression in the CLC cell line, and there was a trend for increased expression in the EMA cell line but no effect in the CLK cell line. Activation of LH receptors increased proliferation in all 3 cell lines, endothelium adhesion in 2 cell lines (CLC, CLK), and transmigration in 2 cell lines (CLK, EMA). LH receptor stimulation using hCG increased LH receptor gene expression in neoplastic canine T lymphocytes and increased cell proliferation, adhesion, and transmigration. These findings may provide a physiologic mechanism for the increased incidence of lymphoma reported in dogs with sustained supraphysiologic LH concentrations.
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