Transcytosis: Crossing Cellular Barriers

Tuma, Pamela L.; Hubbard, Ann L.

doi:10.1152/physrev.00001.2003

Cited by 572 publications

(508 citation statements)

References 607 publications

(409 reference statements)

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“…Decreased bile production has further been implicated in impaired absorption of dietary lipids observed in the alcoholic patient [101].…”

Section: Clinical Implications Of Impaired Protein Traffickingmentioning

confidence: 99%

“…Much of this is due to the fact that an alcoholic often substitutes the calories from ethanol for the calories from food such that he/she becomes malnourished [44,59]. This is further exacerbated by the decreased intestinal absorption of many compounds including dietary fats, fat soluble vitamins, essential amino acids, folic acid, glucose and minerals such as calcium, zinc, iron and magnesium [101]. In general, these defects are not likely due to impaired clathrin-mediated endocytosis.…”

Section: Impaired Clathrin-mediated Internalization Likely Alters Nummentioning

confidence: 99%

Section: Vitamin B 12 and Fat Soluble Vitaminsmentioning

confidence: 99%

“…Unlike many other hydrophobic vitamins, B 12 is internalized via clathrin-mediated mechanisms in the intestine, liver and kidney [101]. In the small intestine, vitamin B 12 associates with intrinsic factor, a small glycoprotein synthesized and secreted by gastric parietal cells [101]. The B 12 -intrinsic factor complex binds enterocytes via its receptor, cubilin, which in turn is complexed to the transmembrane protein, megalin [101].…”

Section: Vitamin B 12 and Fat Soluble Vitaminsmentioning

confidence: 99%

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Alcohol consumption impairs hepatic protein trafficking: mechanisms and consequences

2009

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Alcoholic liver disease is a major biomedical health concern in the United States. Despite considerable research efforts aimed at understanding the progression of the disease, the specific mechanisms leading to alcohol-induced damage remain elusive. Numerous proteins are known to have alcohol-induced alterations in their dynamics. Defining these defects in protein trafficking is an active area of research. In general, two trafficking pathways are affected: transport of newly synthesized secretory or membrane glycoproteins from the Golgi to the basolateral membrane and clathrin-mediated endocytosis from the sinusoidal surface. Both impaired secretion and internalization require ethanol metabolism and are likely mediated by acetaldehyde. Although the mechanisms by which ethanol exposure impairs protein trafficking are not fully understood, recent work implicates alcohol-induced modifications on tubulin or components of the clathrin machinery as potential mediators. Furthermore, the physiological ramifications of impaired protein trafficking are not fully understood. In this review, we will list and discuss the proteins whose trafficking patterns are known to be impaired by ethanol exposure. We will then describe what is known about the possible mechanisms leading to impaired protein trafficking and how disrupted protein trafficking alters liver function and may explain clinical features of the alcoholic patient.

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“…Decreased bile production has further been implicated in impaired absorption of dietary lipids observed in the alcoholic patient [101].…”

Section: Clinical Implications Of Impaired Protein Traffickingmentioning

confidence: 99%

Section: Impaired Clathrin-mediated Internalization Likely Alters Nummentioning

confidence: 99%

Section: Vitamin B 12 and Fat Soluble Vitaminsmentioning

confidence: 99%

Section: Vitamin B 12 and Fat Soluble Vitaminsmentioning

confidence: 99%

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Alcohol consumption impairs hepatic protein trafficking: mechanisms and consequences

2009

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“…11 Clathrin-, lipid raft-, or caveolae-mediated endocytosis is considered as means of transcellular transport. 12 In intestinal cells, endocytosis involves clathrin-coated pits that internalize cargo and deliver it to other cellular destinations. However, transendothelial transport in blood vessels does not conform to this scenario.…”

Section: Introductionmentioning

confidence: 99%

Ablation of MMP9 Gene Ameliorates Paracellular Permeability and Fibrinogen–Amyloid Beta Complex Formation during Hyperhomocysteinemia

Muradashvili

Tyagi

Metreveli

et al. 2014

J Cereb Blood Flow Metab

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Increased blood level of homocysteine (Hcy), called hyperhomocysteinemia (HHcy) accompanies many cognitive disorders including Alzheimer's disease. We hypothesized that HHcy-enhanced cerebrovascular permeability occurs via activation of matrix metalloproteinase-9 (MMP9) and leads to an increased formation of fibrinogen-b-amyloid (Fg-Ab) complex. Cerebrovascular permeability changes were assessed in C57BL/6J (wild type, WT), cystathionine-b-synthase heterozygote (Cbs þ / À , a genetic model of HHcy), MMP9 gene knockout (Mmp9 À / À ), and Cbs and Mmp9 double knockout (Cbs þ / À /Mmp9 À / À ) mice using a dual-tracer probing method. Expression of vascular endothelial cadherin (VE-cadherin) and Fg-Ab complex formation was assessed in mouse brain cryosections by immunohistochemistry. Short-term memory of mice was assessed with a novel object recognition test. The cerebrovascular permeability in Cbs þ / À mice was increased via mainly the paracellular transport pathway. VE-cadherin expression was the lowest and Fg-Ab complex formation was the highest along with the diminished short-term memory in Cbs þ / À mice. These effects of HHcy were ameliorated in Cbs þ / À /Mmp9 À / À mice. Thus, HHcy causes activation of MMP9 increasing cerebrovascular permeability by downregulation of VE-cadherin resulting in an enhanced formation of Fg-Ab complex that can be associated with loss of memory. These data may lead to the identification of new targets for therapeutic intervention that can modulate HHcy-induced cerebrovascular permeability and resultant pathologies.

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Endocytosis: Receptor‐Mediated

Peterson

2008

Wiley Encyclopedia of Chemical Biology

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Specific receptors on the surface of mammalian cells actively internalize cell‐impermeable ligands by the mechanism of receptor‐mediated endocytosis (RME). This process is critical for the acquisition of nutrients, signal transduction, development, neurotransmission, and cellular homeostasis. Binding of ligands to internalizing receptors on the plasma membrane results in clustering of the complex in clathrin‐coated pits or other dynamic membrane regions. Invagination of these regions yields intracellular vesicles that fuse to form membrane‐sealed endosomes. Receptors typically dissociate from ligands in these acidic compartments, which allows the free receptor to cycle back to the cell surface, whereas ligands are often degraded on delivery to lysosomes, which liberates amino acids and other nutrients. By mimicking endogenous ligands, certain protein toxins, viruses, and other pathogens exploit RME to enter the cytoplasm or reach other intracellular destinations. Similarly, artificial delivery systems that mimic ligands or receptors can enhance efficiently the cellular uptake of impermeable molecules, including drugs, proteins, and nucleic acids. Advances in small‐molecule probes, structural biology, and genetic methods are beginning to illuminate the complex mechanisms of this process at the molecular level.

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Transcytosis: Crossing Cellular Barriers

Cited by 572 publications

References 607 publications

Alcohol consumption impairs hepatic protein trafficking: mechanisms and consequences

Alcohol consumption impairs hepatic protein trafficking: mechanisms and consequences

Ablation of MMP9 Gene Ameliorates Paracellular Permeability and Fibrinogen–Amyloid Beta Complex Formation during Hyperhomocysteinemia

Endocytosis: Receptor‐Mediated

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