Caveolae, by virtue of their unique lipid environment, serve as signaling platforms that regulate cellular events. Perturbations in caveolae lipid composition have been shown in vitro to displace proteins from lipid microdomains, thereby altering their functionality and subsequent downstream signaling. Because membrane remodeling may not be accurately represented by using pharmacological treatments and in vitro models, we investigated the in vivo ability of dietary n-3 polyunsaturated fatty acids (PUFA) to alter caveolae lipid environment and the compartmentalization of resident proteins in mouse colonic mucosa. n-3 PUFA were examined for their chemoprotective, membrane lipid-modifying properties. Colonic caveolae in mice fed n-6 or n-3 PUFA enriched diets were characteristically enriched in cholesterol, sphingomyelin, and caveolin-1. n-3 PUFA feeding, compared with n-6 PUFA, significantly altered colonic caveolae microenvironment by increasing phospholipid n-3 fatty acyl content and reducing both cholesterol (by 46%) and caveolin-1 (by 53%), without altering total cellular levels. Concomitantly, localization of caveolae-resident signaling proteins H-Ras and eNOS in colonic caveolae was decreased by n-3 PUFA, by 45 and 56%, respectively. The distribution of non-caveolae proteins K-Ras and clathrin was unaffected. Moreover, EGF-stimulated H-Ras, but not K-Ras activation was significantly suppressed following n-3 PUFA feeding, in parallel with the selective alterations in their microlocalization. These findings reveal a novel modality by which n-3 PUFA remodel membrane microdomains in vivo and thereby alter caveolae protein localization and functionality.

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In nature, pollen grains play a vital role for encapsulation. Many pollen species exist which are often used as human food supplements. Dynamic image particle analysis, scanning electron microscopy, and confocal microscopy analysis confirmed the size, structural uniformity, and macromolecular encapsulation in sunflower pollen, paving the way to explore natural pollen grains for the encapsulation of therapeutic molecules.

A growing body of epidemiological, clinical,

Background: ApoM overexpression in nonhepatic cells generates larger nascent HDLs. Results: Hepatocyte-specific apoM transgenic mice have larger plasma HDLs and hepatocytes that generate larger nascent HDLs and increased S1P secretion. Conclusion: Hepatocyte-specific apoM overexpression facilitates large apoM/S1P-enriched HDL formation by promoting large nascent HDL formation and stimulating sphingolipid synthesis and S1P secretion. Significance: Hepatic apoM regulates HDL and S1P production.