The transformation of a granular cell into a keratinized cell also involves breakdown of the nucleus and other  organelles and thickening of the plasma membrane. This is accompanied by a change in pH, which decreases from  approximately neutral (pH 7.17) in the stratum granulosum to acidic at the surface of the stratum corneum, ranging between pH 4.5 and 6.0.
Desquamation of surface keratinocytes from the stratum corneum is regulated by proteolytic degradation of the cells’ desmosomes.
Cells are regularly exfoliated or desquamated from the surface of the stratum corneum. The continuous exfoliation of surface keratinocytes is a regulated proteolytic process that involves degradation of the cells’ desmosomes. The human kallikrein-related serine peptidases such as KLK5, KLK7, and KLK14 cause cleavage of desmosomes in a pH-dependent manner. A physiological serine protease  inhibitor, lymphoepithelial Kazal-type inhibitor (LEKTI), through its interactions with KLKs in neutral pH, prevents desmosomal cleavage. However, as pH decreases in more superficial portions of the stratum corneum as described, LEKTI progressively releases KLKs at the lower pH, thus allowing KLKs to degrade the desmosomes and cause keratinocyte release (see Fig 15.4). Under normal condition, the process allows a controlled renewal of the epidermis by means of its pH gradient. Recently, pathogenic mutations were identified in the gene called serine protease inhibitor Kazal-type 5 (SPINK5), which encodes LEKTI. Netherton syndrome, a rare genetic disorder associated with a defective SPINK5 gene, is characterized by decreased skin barrier function, generalized redness of the skin (erythroderma), and scaling.
Lamellar bodies contribute to the formation of the inter-cellular epidermal water barrier.
An epidermal water barrier is essential for mammalian “dry” epithelia and is responsible for maintaining body homeostasis. The barrier is established primarily by two factors in terminally differentiating keratinocytes: (1) deposition of insoluble proteins on the inner surface of the plasma membrane and (2) a lipid layer that is attached to the outer surface of the plasma membrane.
As the keratinocytes in the stratum spinosum begin to produce keratohyalin granules, they also produce membrane-bounded lamellar bodies (membrane-coating granules). They are tubular or ovoid-shaped membrane-bound organelles that are unique to mammalian epidermis. Spinous and granular cells synthesize a heterogenous mixture of pro-barrier lipids and their respective lipid-processing enzymes such as glycosphingolipids, phospholipids, ceramides, acidic sphingomyelinase, and secretory phospholipase A2 (Fig. 15.5); this mixture is assembled into lamellar bodies in the Golgi apparatus. In addition, lamellar bodies contain proteases (i.e., SC chymotryptic enzyme, cathepsin D, acid phosphatase, glycosidases, protease inhibitors). The contents of the granules are then secreted by exocytosis into the intercellular spaces between the stratum granulosum and stratum corneum. The organization of these intercellular lipid lamellae is responsible for the formation of the  epidermal water barrier (Fig. 15.6). In addition to their major role in the formation of barrier homeostasis, lamellar bodies are also pH 4.5–5.3pH 6.8–7.5