Cholesterol and Sphingolipids transport / Recycling to plasma membrane in lung (normal and CF)

Cholesterol and Sphingolipid transport/ Recycling to plasma membrane in lung (normal and CF)

In lungs, Cholesterol and Sphingolipids move from early endosomes to the endocytic recycling compartment (ERC) via a Rab-dependent mechanism. Oligomerization of EH domain-containing proteins 1 and 3 (EHD1 and EHD3) is necessary for attraction of Rab11 family interacting protein 2 (Rab11-FIP2). These proteins interact with member RAS oncogene family Rab-11A and their interactions regulate traffic of cargo and lipids through perinuclear recycling endosomes [1], [2]. ERC is thus one of the most Cholesterol-rich compartments in the cell [3].

Cholesterol can move from the plasma membrane to the ERC and back by a non-vesicular, ATP-independent process. Sterol carrier protein 2 (SCPX(SCP2)) carries Cholesterol from internal membranes to plasmalemma, specifically to caveolae-lipid rafts [1], [4], [5].

Soluble cytosolic sterol carrier proteins transport Cholesterol to the inner leaflet of the plasma membrane. ATP-binding cassette family member 1 (ABCA1) activity is crucial for the maintenance of the normal lung lipid composition [6], [7]. ATP-binding cassette, sub-family G member 1 and sub-family A member 7 (ABCG1 and ABCA7) transports Cholesterol from the inner to outer leaflets enriching the latter [8], [9], [10], [11], [12]. Specific binding of Apolipoprotein A-I (APOA1) to ABCA1 involves a direct molecular interaction. APOA1 binding to ABCA1 promotes efflux of cellular Cholesterol and phospholipids, likely as a result of coordinated specific transmembrane transport of both lipids by ABCA1 [11], [13], [14].

Sphingolipids also recycle via the endocytic recycling compartment [15].

References:

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