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Low back pain is second only to cancer in terms of socioeconomic burden in the U.S., but current treatments are highly invasive and fail to target the underlying cellular mechanisms of intervertebral disc (IVD) degeneration. In degeneration, the cartilaginous end plate (CEP) becomes calcified, however the mechanisms are not well understood. In diseases such as osteoarthritis, a proposed mechanism is the recapitulation of developmental processes and we suggest that in degeneration, CEP cells undergo hypertrophic differentiation similar to endochondral ossification. The aim of this study was to determine if CEP cells can undergo hypertrophic differentiation, leading to angiogenesis. Human CEP cells (hCEPs) were isolated from autopsy and pellet cultured. For 21 days, pellets were cultured in either chondrogenic or hypertrophic (10% FBS or CHIR99021, a wnt agonist) media in 5% oxygen, after which samples were used for viability, histology, qRT-PCR, DMMB proteoglycan assay, and generation of conditioned media (CM). Soluble factors from CM generated after 21 days was pooled, and a HUVEC tubular formation assay ran. Tubular length was assessed using Image J plug in, Angiogensis Analyzer. No significant decreases in viability were seen in the chondrogenic control group. QRT-PCR showed a decrease of chondrogenic marker, COL2, in both hypertrophy groups compared to the chondrogenic group. Hypertrophic markers MMP13 and IHH displayed increases in the hypertrophy groups. Increases were also seen in the angiogenic and pain related markers, VEGF-A, TAC1, and NGF in the hypertrophy groups. DMMB assay and histological results show decreases in proteoglycans in the hypertrophy groups. HUVEC tubular formation assay showed that both hypertrophy groups increased the total length of tubules. This study sought to determine the underlying cellular mechanisms of low back pain and suggests that human CEPs have the ability to undergo hypertrophic differentiation similar to articular chondrocytes during OA, with subsequent angiogenesis and neoinnervation, and may be implicated in the process of IVD degeneration.