Lamellar granule

Lamellar granules (otherwise known as lamellar bodies, keratinosomes or Odland bodies) are secretory organelles found in type II pneumocytes and keratinocytes. They are oblong structures, appearing about 300-400 nm in width and 100-150 nm in length in transmission electron microscopy images. Lamellar granules fuse with the cell membrane and release their contents into the extracellular space.[1]

Contents

Role in Lungs

In pneumocytes, the choline-based phospholipids that are stored in the lamellar bodies serve as pulmonary surfactant after being released from the cell.

Role in Epidermis

In the stratum granulosum layer of the epidermis, lamellar bodies are secreted from keratinocytes, resulting in the formation of an impermeable, lipid-containing membrane that serves as a water barrier and is required for correct skin barrier function. These granules release components that are required for skin shedding (desquamation) in the uppermost epidermal layer, the stratum corneum.[2] These components include lipids (eg. glucosylceramides), hydrolytic enzymes (eg. proteases, acid phosphatases, glucosidases, lipases) and proteins (eg. corneodesmosin).[3] Lamellar granules have been observed to contain distinct aggregates of the secreted components glucosylceramide, cathepsin D, KLK7, KLK8 and corneodesmosin. Transportation of molecules via lamellar granules is thought to prevent enzymes from interacting with their relevant substrates or inhibitors prior to secretion.[3]

Recent work suggests that lamellar granules form a continuous membranous structure with the trans-Golgi network

Lamellar body secretion and lipid structure is abnormal in the epidermis of patients with Netherton syndrome, a skin disorder characterised by chronic inflammation and universal pruritis (itch).[4]

References

  1. ^ Ishida-Yamamoto A, Kishibe M. (Mar 2011). "Involvement of corneodesmosome degradation and lamellar granule transportation in the desquamation process.". Med Mel Morphol. 44 (1): 1–6. PMID 21424930. 
  2. ^ Descargues P, Deraison C, Bonnart C, Kreft M, Kishibe M, Ishida-Yamamoto A, Elias P, Barrandon Y, Zambruno G, Sonnenberg A, Hovnanian A. (Jan 2005). "Spink5-deficient mice mimic Netherton syndrome through degradation of desmoglein 1 by epidermal protease hyperactivity.". Nat Genet 37 (1): 56–65. PMC 15619623. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=15619623. 
  3. ^ a b Ishida-Yamamoto A, Simon M, Kishibe M, Miyauchi Y, Takahashi H, Yoshida S, O'Brien TJ, Serre G, Iizuka H. (May 2004). "Epidermal lamellar granules transport different cargoes as distinct aggregates.". J Invest Dermatol. 122 (5): 1137–44. PMC 15140216. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=15140216. 
  4. ^ Fartasch M, Williams ML, Elias PM. (Jul 1999). "Altered lamellar body secretion and stratum corneum membrane structure in Netherton syndrome: differentiation from other infantile erythrodermas and pathogenic implications.". Arch Dermatol. 135 (7): 823–32. PMID 10411158. 

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