Cytoplasmic crescents

The extent to which membranes isolated from washed lipid globules originate from the apical plasma membrane, with perhaps some contribution from mature secretory vesicle membrane, can be an important consideration. Any intracellular membranes, contained in cytoplasmic crescents, will be present in preparations obtained by any of the meth-... 

Figure 4.7. Electron micrograph of a milk fat globule in the alveolar lumen that has a large cytoplasmic crescent entrained between the globule and the surrounding membrane. This crescent contains secretory vesicles, ribosome-studded vesicles of apparent endoplasmic reticulum origin, and an abundant amount of particulate material. Bar = 2 pm.

Some of the enzymes of the MFGM, such as 5 -nucleotidase, adenosine triphosphatase and phosphodiesterase I, are known to be enriched in plasma membranes. However, other enzymes found in the MFGM are known constituents of intracellular membranes or are cytosolic. Why some of these are present in the MFGM remains to be explained some may possibly originate from material entrained in cytoplasmic crescents and therefore are not true MFGM constituents. Perhaps some enzymes become... 

Huston, G.E., Patton, S. 1990. Factors related to the formation of cytoplasmic crescents on milk fat globules. J. Dairy Sci. 73, 2061-2066. 

In some milk fat globules, small aqueous compartments are located beneath the membrane bilayer, which have been termed cytoplasmic crescents (Huston and Patton, 1990). Whether or not this cytoplasmic inclusion provides some benefit is unknown. Yet, as this aqueous compartment is protected from the bulk serum phase by the MFGM, constituents located therein are presumably afforded some protection, at least initially, from gastric hydrolysis. Huston and Patton (1990) found crescents in all samples of milk they examined, and they were more prevalent in human (7.3% of globules), than in bovine (1% of globules) milk. Furthermore, there was considerable individual and diurnal variation. The structure of a cytoplasmic inclusion, surrounded by an intact plasma membrane on one side and a fat globule surface on the other, may allow certain labile constituents to be protected until they reach their proper site of bioactivity. At this point it is not known whether the crescents have a purpose or are simply the result of inefficiencies in the secretion process. As it is possible to isolate milk preparations enriched in cytoplasmic crescents, there is an opportunity to determine the nature of the materials found within. This unusual biocompartment may prove to be a model of food structure for biodelivery. 

Epithelial cells express but do not apically localize Pins, and do not express Insc. We have previously shown that ectopically expressed Insc localizes to the apical cortex in wild-type epithelial cells (Kraut et al 1996). Interestingly, ectopic Insc expression causes Pins, which is normally localized to the lateral cortex, to localize to the apical cortex. Conversely, apical localization of ectopically expressed Insc is dependent on pins. Insc ectopically expressed in Pins- epithelial cells does not localize as an apical crescent it adopts a cytoplasmic distribution which is enriched towards the apical side of the cell during interphase and is undetectable during mitosis, presumably due to rapid degradation. This instability of ectopically expressed Insc may be why the 90° rotation in the mitotic spindles which occurs as a consequence of Insc ectopic expression in the wild-type epithelial cells no longer occurs when Insc is expressed in Pins-embryos. These results indicate that Insc is necessary and sufficient for the recruitment of Pins to the apical cortex of wild-type epithelial cells. 

Kawaguchi H, Ito K. Antineutrophil cytoplasmic anti-body-positive crescentic glomerulonephritis associated with propylthiouracil therapy. Acta Paediatr Jpn... 

Huston and Patton (1990) suggested that an abnormality in the protein coat along the cytoplasmic face of the apical plasma membrane may be responsible for the phenomenon of crescent formation. Inadequate amounts of proteins forming this coat or abnormalities in the distribution of the coat complex may interfere with adhesion of the membrane to the droplet. 

Falk RJ, Jennette JC. Anti-neutrophil cytoplasmic autoantibodies with specificity for myeloperoxidase in patients with systemic vasculitis and idiopathic necrotizing and crescentic glomerulonephritis. 

While not yet conclusive, studies on the gray crescent described above may provide yet another example of substances accumulated within the GV during oogenesis which become effective only after dispersal into the cytoplasm. It would be most significant if these or other nuclear products could be related to the cytoplasmic localizations referred to earlier. Whether any of the examples yet discussed falls into this category remains to be seen and will depend to a large- extent on continued attempts to identify the nature of the active materials and their mode of action. This alone requires continued interest in the period of maturation. However, it is possible that the various factors described above are involved in more generalized metabolic functions which, while necessary to normal development, are not directly involved in the differentiation of specific cell types. 

D Cmz D, Cbesser AM, Ligbtowler C, et al. Antineutrophil cytoplasmic antibodypositive crescentic glomemlonephritis associated with anti-thyroid drug treatment. BrJ Rheumatol 1995 34(11) 1090-1091. 

Vogt BA, Kim Y, Jennette JC, et al. Antineutrophil cytoplasmic autoantibodypositive crescentic glomerulonephritis as a complication of treatment with propylthiouracil in children. J Pediatr 1994 124 986-988. 

Falk RJ, Jennette JC. Anti-neutrophil cytoplasmic autoantibodies with specificity for myeloperoxidase in patients with systemic vasculitis and idiopathic necrotizing and crescentic glomerulonephritis. N Engl J Med 1988 318 1651-1657. Goldschmeding R, van der Schoot CE, ten Bokkel Huinink D, et al. Wegener s granulomatosis autoantibodies identify a novel diisopropylfluorophosphate-binding protein in the lysosomes of normal human neutrophils. J Clin Invest 1988 4 1577-15879. 

Kain R, Matsui K, Exner M, et al. A novel class of autoantigens of anti-neutrophil cytoplasmic antibodies in necrotizing and crescentic glomerulonephritis the lysosomal membrane glycoprotein h-lamp-2 in neutrophil granulocytes and a related membrane protein in glomerular endothelial cells. J Exp Med 1995 181 585-597. Savage CO, Williams JM. Anti endothelial cell antibodies in vasculitis. J Am Soc Nephrol 2007 18 2424-2426. 

Ruth AJ, Kitching AR, Kwan RY, et al. Anti-neutrophil cytoplasmic antibodies and effector CD4+ cells play nonredundant roles in anti-myeloperoxidase crescentic glomerulonephritis. J Am Soc Nephrol 2006 17 1940-1949. 

Yang G, Tang Z, Chen Y, et al. Antineutrophil cytoplasmic antibodies (ANCA) in Chinese patients with anti-GBM crescentic glomerulonephritis. Chn Nephrol 2005 ... 

Urinary tract A case report was published on anti-neutrophil cytoplasmic antibody (ANCA)-positive pauci-immxme glomerulonephritis during febuxostat treatment. A 63-year-old African started treatment with febuxostat (dose not reported) because he had a history of chronic asymptomatic hyperuricemia which was not adequately controlled by allopurinol therapy. After 6 months of febuxostat therapy he developed AKI, characterised by acute renal failure, nephritic syndrome, proteinuria, microscopic haematuria and aseptic leukocyturia. Within 48 h after discontinuation of febuxostat, serum creatinine levels improved, although nephritic syndrome remained. ANCA-positive pauci-immune glomerulonephritis was confirmed by renal biopsy revealing diffuse crescentic necrotizing glomerulonephritis [60 ]. 

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