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. Author manuscript; available in PMC: 2017 Mar 17.
Published in final edited form as: Biochim Biophys Acta. 2015 Feb 14;1848(10 Pt B):2677–2684. doi: 10.1016/j.bbamem.2015.02.004

Figure 1. Proton secretion by bone-resorbing osteoclasts.

Figure 1

To dissolve bone minerals, mature osteoclasts release protons (H+) and chloride ions (Cl−) into the resorption lacunae via the plasma membrane (a3 isoform) vacuolar H+-ATPase proton pump [23] and chloride ion-proton anti-porter ClC-7 [24], acidifying the resorption lacunae to a pH of 4.5 [7]. Concomitantly, the lysosomal cysteine peptidase cathepsin K [25] degrades bone matrix including type I collagen.

RANKL stimulates osteoclastogenesis and bone resorption and prolongs survival by inhibiting apoptosis. CAII: Carbonic anhydrase II, ClC7: Plasma membrane chloride ion-proton anti-porter, RANK: receptor activation of NF-κB, RANKL: receptor activation of NF-κB ligand, V-H+-ATPase: Plasma membrane (a3 isoform) vacuolar H+-ATPase proton pump,