Table 1.

Other membrane receptors associated or implicated with osteoarthritis, but with less well characterized roles in joint function.

Receptor	Long name or descriptor	Context
LRP-1	Low-density lipoprotein receptor-related protein (aka apolipoprotein E receptor, CD91), reviewed by May et al. (2007)	Drives rapid endocytosis of ADAMTS-5; LRP-1 is down-regulated in human articular cartilage from OA patients. Transcript abundance increased in damaged vs. intact cartilage (Geyer et al., 2009)
InsR/IGF-R	Insulin Receptors and Insulin like Growth factor receptors	Both InsR/ILGF-R are decreased in chondrocytes from patients with OA (Rosa et al., 2011) and the IGF-I peptide itself increases expression of COL2A1 in articular chondrocytes (Renard et al., 2012)
TLR	Toll-like receptor proteins (members of the interleukin receptor family), with many ligands such as heat shock proteins and hyaluronic acid oligomers. Includes TLR1−11 (Akira and Takeda, 2004)	Are more commonly found on inflammatory cells and serve to initiate inflammatory responses/innate immunity. TLR1−9 identified in cartilage and are differentially expressed in OA cartilage (Kuroki et al., 2010; Barreto et al., 2013; Yang et al., 2013). Polymorphism of the TLR3 and TLR9 promoted associate with severe OA (Su et al., 2012; Yang et al., 2013) and “alarmins” accelerate catabolism in OA cartilage in a TLR4 dependent mechanism (Schelbergen et al., 2012)
TGFβ-RII	Transforming growth factor β receptor 2	TGFβ-RII expression decreases with age and potentially predisposes older people to OA (Bauge et al., 2013) and its genetic deletion increases OA in mice (Zhen et al., 2013)
PPARγ-R	Peroxisome Proliferator-Activated Receptor-γ, a nuclear receptor	PPARγ-R is down-regulated in both human OA (Afif et al., 2007) and in several OA models (Fahmi et al., 2011) including the spontaneous Guinea-pig model (Nebbaki et al., 2013). In some cases this is secondary to Erg-1 mediated IL-1 (Nebbaki et al., 2012) and/or TLR4 activation (Chen et al., 2013)
MC-R	Melanocortin peptide receptors, for example MC1-R and MC2-R. Endogenous pharmacological activators include α-melanocyte-stimulating hormone (α-MSH), pro-opiomelanocortin (POMC) and adrenocorticotrophin (ACTH)	MC1, MC2, MC5, and ligand POMC transcribed in cartilage, induces expression of several ECM components and pro-inflammatory cytokines (Grässel et al., 2009), but can also mediate chondro- and cartilage- protective effects of neuropeptides such as α-MSH, POMC in both in vitro and rat in vivo models of OA (Shen et al., 2011; Kaneva et al., 2012)
CD36	A pattern recognizing receptor (Silverstein and Febbraio, 2009). Aka “thrombospondin receptor”	CD36 is well known to increase in OA (Pfander et al., 2000), however, recent data show it is also able to suppress catabolic activity and serves as a marker of hypertrophy (Cecil et al., 2009)
PTH1-R	Parathyroid receptor-1	PTH1-R expression is decreased in rabbits with ACL section induced OA (Becher et al., 2010)
Ob-R	Leptin receptor	With onset of OA there is a switch from adipokine synthesis to receptor synthesis (Francin et al., 2011). Leptin itself enhances production of catabolic MMP enzymes in OA cartilage (Iliopoulos et al., 2007; Koskinen et al., 2011). It is believed that leptin may mediate the pro-OA effects of obesity rather than simply the increased load observed in weight baring joints
CD44	Hyaluronan receptor (aka HA-R)	Activation inhibits expression of ADAMTS4 (aggrakinase-1) and MMP-13 in [osteoarthritic] chondrocytes (Yatabe et al., 2009; Julovi et al., 2011), although some hyaluronan effects could be mediated through the TLRs (see below)
FGF-R	Fibroblast growth factor (FGF) receptors, family includes FGFR1, 2, 3, and 4. Sensitive to the 22 member FGF family	FGFR-3 in has been shown to mediate chondroprotective of FGF18 (Ellman et al., 2013). Please see Vincent (2012) for discussion of the role of FGF in OA.