Colchicine inhibition of plasma protein release from rat hepatocytes.

Redman, Colvin M.; Banerjee, Dev; Howell, Kathryn E.; Palade, G E

doi:10.1083/jcb.66.1.42

Cited by 292 publications

(149 citation statements)

References 42 publications

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“…When administered sys temically, vinblastine disrupts micro tubules (Ekholm et al, 1974;Ericson, 1980; 1981) . and interferes with secretion (Redman et aL, 1975;Ericson, 1980;Williams, 1981). The results are identical to those produced by colcemid (Karim and Warshawsky, 1979;Nishikawa and Kitamura, 1982).…”

Section: Response Of the Enamel Organ And Ename! To Drilling Proceduressupporting

confidence: 69%

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In vivo experimentation on rat incisor enamel organs through a surgical window

McKee

Warshawsky

1984

Anat. Rec.

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Experimental agents administered systemically are costly and often toxic to animals. An in vivo technique has been developed whereby a surgical window in the alveolar bone allows selected areas of the rat incisor enamel organ and underlying enamel to be exposed to various drugs, radiolabeled molecules, and molecular weight markers. Sherman rats weighing 100 gm were anesthetized and the inferior surface of each hemimandible was surgically exposed. A slow‐speed dental hand drill was used to drill a small hole through the alveolar bone overlying the secretion or maturation zones of the enamel organ. The wound was closed and during recovery the mechanical trauma to the underlying tissue moved away from the hole due to the continuous eruption of the tooth. Two to 5 days later the hole was reexposed and microinjections of 3H‐proline, 125I‐salmon calcitonin, vinblastine sulphate, and normal saline (as control) were administered through the hole with a micro‐manipulator and a microliter syringe. Radioautographic detection of 3H‐proline incorporation in secretory ameloblasts and enamel at 10 minutes, 30 minutes, 1 hour, 4 hours, 1 day, and 2 days after microinjection was identical to that obtained previously by systemic injection. Two hours after microinjection of vinblastine sulphate the cellular response was again identical to that following systemic injection; 125I‐salmon calcitonin (M.W. ∼ 3,600D) was used as a molecular weight marker and was seen to diffuse into the enamel of the maturation zone at 10 minutes after microinjection. This study has demonstrated the feasibility of this new technique for experimentation on rat incisor enamel organs.

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Section: Response Of the Enamel Organ And Ename! To Drilling Proceduressupporting

confidence: 69%

“…The vinka alkaloid vinb1astine sulphate has beEn shown to disrupt micro tubules (Ekho1m et 'Ericson, 1980j . Williams, 1981), and to Interfere with secretion (Redman et al, 1975;Ericson, 198~Wil1iams, 1981). Vinb1astine binds to the microtubule subunit tubulin, preventing polymerization, and results in a 10s,8 of micro-…”

mentioning

confidence: 99%

In vivo experimentation on rat incisor enamel organs through a surgical window

McKee

Warshawsky

1984

Anat. Rec.

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“…In addition, since colchicine has been shown to inhibit secretion of a variety of plasma proteins by the cells in which they are synthesized (14)(15)(16)(17), the effect of administration of this drug upon cellular localization of CRP during acute inflammation was investigated.…”

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confidence: 99%

Control of the acute phase response. Demonstration of C-reactive protein synthesis and secretion by hepatocytes during acute inflammation in the rabbit.

Kushner¹,

Feldmann²

1978

The Journal of Experimental Medicine

198

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To determine the cell of origin of C-reactive protein (CRP) and to cast light on the mechanisms leading to the acute phase response, we used an immunoenzymatic technique to visualize this protein in livers from rabbits at intervals after intramuscular injection of turpentine. CRP was detected only in hepatocytes. 8 h after turpentine injection, CRP was demonstrated in occasional periportal hepatocytes. With time, larger numbers of positive cells were detected successively in perilobular, midlobular, and centrilobular areas. On electron microscopy, CRP was detected in rough endoplasmic reticulum (RER), smooth endoplasmic reticulum (SER), and Golgi apparatus (GA). When colchicine was administered to inhibit cellular secretion of CRP, intensity of reaction and number of CRP-containing hepatocytes were substantially greater than without colchicine, but the sequence of intralobular distribution was similar. At peak serum response 38 h after turpentine injection, CRP could be demonstrated in most hepatocytes. Electron microscopic studies showed accumulation of CRP on membranes and lumina of RER, SER, GA, and in cytoplasmic vacuoles. These findings indicate that CRP is produced by progressively increasing numbers of hepatocytes after inflammatory stimulus and suggest that a mediator, acting initially in portal zones, is responsible for recruitment of cells to CRP production.

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“…Microtubular inhibitors such as colchicine and vinblastine have been shown to inhibit secretion of protein and lipid from liver into blood plasma [34,43,63,73]. Since it is known that these agents in addition to their specific binding to tubulin exhibit unspecific binding to subcellular membranes [72], the effect of colchicine and vinblastine on the Ca 2 + induced fusion of isolated secretory vesicles was studied.…”

Section: Effect Of Microtubular Inhibitorsmentioning

confidence: 99%

“…Secretion of lipids and proteins from the hepatocyte into blood plasma was found to be inhibited by these substances [34,43,63,73]. On the other hand, colchicine is known to bind unspecifically to membranes isolated from rat and mouse liver [72], and therefore an effect on the membrane level has to be taken into account.…”

Section: Effect Of Various Substances On Ca 2 +-Induced Fusionmentioning

confidence: 99%

Fusion of secretory vesicles isolated from rat liver

Gratzl

Dahl

1978

J. Membrain Biol.

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Summary. Secretory vesicles isolated from rat liver were found to fuse after exposure to Ca 2 +. Vesicle fusion is characterized by the occurrence of twinned vesicles with a continuous cleavage plane between two vesicles in freeze-fracture electron microscopy. The number of fused vesicles increases with increasing Ca 2 +-concentrations and is half maximal around 10 -6 M. Other divalent cations (Ba 2+, Sr 2+, and Mg 2+) were ineffective. Mg 2+ inhibits Ca2+-induced fusion. Therefore, the fusion of secretory vesicles in vitro is Ca z+ specific and exhibits properties similar to the exocytotic process of various secretory cells.Various substances affecting secretion in vivo (microtubular inhibitors, local anesthetics, ionophores) were tested for their effect on membrane fusion in our system.The fusion of isolated secretory vesicles from liver was found to differ from that of pure phospholipid membranes in its temperature dependence, in its much lower requirement for Ca 2+, and in its Cag+-specificity. Chemical and enzymatic modifications of the vesicle membrane indicate that glycoproteins may account for these differences.Membrane fusion is an essential event in a variety of cell functions such as cell fusion, uptake of extracellular material (endocytosis) and release of cell products (exocytosis). Elucidation of the molecular mechanism of membrane fusion has been hampered by the lack of suitable systems for studying this process. Studies with intact cells have not yielded data which lead to ready interpretation concerning subcellular processes. On the other hand, studies with artificial membranes may be only tangentially related to the fusion of biological membranes.Recently our group investigated the fusion of isolated biological membranes [16,17,31,33,69,74]. We observed that Ca 2+ specifically induces the fusion of isolated secretory vesicles in a buffered sucrose medium.Intervesicular fusion of secretory vesicles, as well as the interaction between the cell membrane and the vesicle membrane, was observed in a variety of secretory cells [2,3,6,18,29,39,53,65]. Douglas [20] showed that in "compound exocytosis" by mast cells an external stimulus initiates fusion between secretory vesicle membranes and the

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Colchicine inhibition of plasma protein release from rat hepatocytes.

Cited by 292 publications

References 42 publications

In vivo experimentation on rat incisor enamel organs through a surgical window

In vivo experimentation on rat incisor enamel organs through a surgical window

Control of the acute phase response. Demonstration of C-reactive protein synthesis and secretion by hepatocytes during acute inflammation in the rabbit.

Fusion of secretory vesicles isolated from rat liver

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