Decorin-loaded poly lactic-co-glycolic acid nanoparticles modified by anti-alpha fetoprotein antibody: preparation, proliferation inhibition and induced apoptosis effects on HepG2 cells <i>in vitro</i>

Yang, Qiaoli; Wang, Shuyue; Wang, Yuan; Qu, Yane; Xue, Jinmei; Mi, Yang; Wang, Yanhong; Luo, Xuguang; Deng, Zhihua; Wang, Guiqin

doi:10.1111/jphp.12695

Cited by 4 publications

(3 citation statements)

References 23 publications

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“…However, decorin at other concentrations did not affect proliferation, therefore, the results of viability assay of these concentrations of decorin have not been influenced by proliferation. The ability of decorin to differentially regulate the cell proliferation is well known for many years [30] and the anti-proliferative effects of decorin are considered to be involved in its anti-cancer effects [31,32]. On the other hand, decorin has been shown to promote the proliferation of myoblasts [33,34] and that gene transfer of decorin in vivo promotes mice skeletal muscle regeneration and accelerates muscle healing after injury [35].…”

Section: Discussionmentioning

confidence: 99%

Decorin Protects Cardiac Myocytes against Simulated Ischemia/Reperfusion Injury

et al. 2020

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Search for new cardioprotective therapies is of great importance since no cardioprotective drugs are available on the market. In line with this need, several natural biomolecules have been extensively tested for their potential cardioprotective effects. Previously, we have shown that biglycan, a member of a diverse group of small leucine-rich proteoglycans, enhanced the expression of cardioprotective genes and decreased ischemia/reperfusion-induced cardiomyocyte death via a TLR-4 dependent mechanism. Therefore, in the present study we aimed to test whether decorin, a small leucine-rich proteoglycan closely related to biglycan, could exert cardiocytoprotection and to reveal possible downstream signaling pathways. Methods: Primary cardiomyocytes isolated from neonatal and adult rat hearts were treated with 0 (Vehicle), 1, 3, 10, 30 and 100 nM decorin as 20 h pretreatment and maintained throughout simulated ischemia and reperfusion (SI/R). In separate experiments, to test the mechanism of decorin-induced cardio protection, 3 nM decorin was applied in combination with inhibitors of known survival pathways, that is, the NOS inhibitor L-NAME, the PKG inhibitor KT-5823 and the TLR-4 inhibitor TAK-242, respectively. mRNA expression changes were measured after SI/R injury. Results: Cell viability of both neonatal and adult cardiomyocytes was significantly decreased due to SI/R injury. Decorin at 1, 3 and 10 nM concentrations significantly increased the survival of both neonatal and adult myocytes after SI/R. At 3nM (the most pronounced protective concentration), it had no effect on apoptotic rate of neonatal cardiac myocytes. No one of the inhibitors of survival pathways (L-NAME, KT-5823, TAK-242) influenced the cardiocytoprotective effect of decorin. MYND-type containing 19 (Zmynd19) and eukaryotic translation initiation factor 4E nuclear import factor 1 (Eif4enif1) were significantly upregulated due to the decorin treatment. In conclusion, this is the first demonstration that decorin exerts a direct cardiocytoprotective effect possibly independent of NO-cGMP-PKG and TLR-4 dependent survival signaling.

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Section: Discussionmentioning

confidence: 99%

Decorin Protects Cardiac Myocytes against Simulated Ischemia/Reperfusion Injury

et al. 2020

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“…Engineering nanoparticles functionalized with or decorated by binding epitopes may be one potential strategy to increase penetrability. For example, decorin, a member of the small leucine-rich proteoglycans, plays an important function in tissue assembly and ECM remodeling, negatively regulates TGFβ, and has been previously shown to successfully load into PLGA NP …”

Section: Nanotechnologymentioning

confidence: 99%

“…For example, decorin, a member of the small leucine-rich proteoglycans, plays an important function in tissue assembly and ECM remodeling, 116 negatively regulates TGFβ, 117 and has been previously shown to successfully load into PLGA NP. 118 2.2.2.2. Immune-Suppressive Barriers.…”

Section: Improving Deliverymentioning

confidence: 99%

Engineering in Medicine To Address the Challenge of Cancer Drug Resistance: From Micro- and Nanotechnologies to Computational and Mathematical Modeling

et al. 2020

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Drug resistance has profoundly limited the success of cancer treatment, driving relapse, metastasis, and mortality. Nearly all anticancer drugs and even novel immunotherapies, which recalibrate the immune system for tumor recognition and destruction, have succumbed to resistance development. Engineers have emerged across mechanical, physical, chemical, mathematical, and biological disciplines to address the challenge of drug resistance using a combination of interdisciplinary tools and skill sets. This review explores the developing, complex, and under-recognized role of engineering in medicine to address the multitude of challenges in cancer drug resistance. Looking through the "lens" of intrinsic, extrinsic, and drug-induced resistance (also referred to as "tolerance"), we will discuss three specific areas where active innovation is driving novel treatment paradigms: (1) nanotechnology, which has revolutionized drug delivery in desmoplastic tissues, harnessing physiochemical characteristics to destroy tumors through photothermal therapy and rationally designed nanostructures to circumvent cancer immunotherapy failures, (2) bioengineered tumor models, which have benefitted from microfluidics and mechanical engineering, creating a paradigm shift in physiologically relevant environments to predict clinical refractoriness and enabling platforms for screening drug combinations to thwart resistance at the individual patient level, and (3) computational and mathematical modeling, which blends in silico simulations with molecular and evolutionary principles to map mutational patterns and model interactions between cells that promote resistance. On the basis that engineering in medicine has resulted in discoveries in resistance biology and successfully translated to clinical strategies that improve outcomes, we suggest the proliferation of multidisciplinary science that embraces engineering.

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Biological toxicity and environmental hazards associated with PLGA nanoparticles

Stromberg¹,

Jacobsen²,

Kocheril³

et al. 2023

Poly(lactic-Co-Glycolic Acid) (PLGA) Nanoparticles for Drug Delivery

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Decorin-loaded poly lactic-co-glycolic acid nanoparticles modified by anti-alpha fetoprotein antibody: preparation, proliferation inhibition and induced apoptosis effects on HepG2 cells in vitro

Abstract: These studies revealed that these nanoparticles were capable of specifically targeting the HepG2 cells and inhibiting the proliferation and they induce apoptosis of HepG2 cells in vitro, which was in a dose- and time-dependent manner.

Cited by 4 publications

References 23 publications

Decorin Protects Cardiac Myocytes against Simulated Ischemia/Reperfusion Injury

Decorin Protects Cardiac Myocytes against Simulated Ischemia/Reperfusion Injury

Engineering in Medicine To Address the Challenge of Cancer Drug Resistance: From Micro- and Nanotechnologies to Computational and Mathematical Modeling

Biological toxicity and environmental hazards associated with PLGA nanoparticles

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