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Updated: Dec 25, 2025
Accessing the Cytotoxicity and Cell Response to Biomaterials
Published on: July 8, 2021
Seaweed Porphyra yezoensis polysaccharides with different molecular weights inhibit hydroxyapatite damage and
Ling-Hong Huang1, Hong Liu, Jia-Yun Chen
1Institute of Biomineralization and Lithiasis Research, Jinan University, Guangzhou 510632, China. toyjm@jnu.edu.cn.
Insights
Porphyra yezoensis polysaccharides (PYPs) protect against vascular calcification by reducing hydroxyapatite (HAP) crystal damage to cells. Low molecular weight PYPs, especially PYP4, showed the best results in inhibiting calcification and cell damage.
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Vascular calcification (VC) is a significant complication in cardiovascular and chronic kidney diseases.
- Hydroxyapatite (HAP) crystal deposition on vascular smooth muscle cells causes damage and promotes osteogenic transformation, contributing to VC.
- Current therapeutic strategies for VC are limited, highlighting the need for novel treatments.
Purpose of the Study:
- To investigate the protective effects of different molecular weights of Porphyra yezoensis polysaccharides (PYPs) against HAP-induced vascular calcification.
- To evaluate the impact of PYPs on HAP crystal toxicity, cell viability, and osteogenic differentiation in vitro.
- To assess the efficacy of PYPs in an in vivo model of chronic renal failure-induced VC.
Main Methods:
- Four molecular weights of PYPs (PYP1-PYP4) were used to coat HAP crystals.
- In vitro studies involved assessing HAP toxicity on A7R5 cells, including cell viability, lactate dehydrogenase release, active oxygen levels, and cell necrosis.
- In vivo studies utilized an adenine-induced chronic renal failure (CRF) mouse model to evaluate the effect of PYP4 on aortic calcification and renal function markers.
Main Results:
- PYPs effectively reduced HAP-induced damage to A7R5 cells, increasing cell viability and decreasing markers of cell damage and necrosis.
- Low molecular weight PYPs exhibited superior protective effects compared to high molecular weight PYPs.
- PYPs inhibited HAP-induced osteogenic transformation, reducing alkaline phosphatase (ALP) activity and the expression of key bone-related genes.
- In vivo, PYP4 significantly reduced aortic calcium content and improved renal function markers (serum creatinine, phosphorus, BUN) in CRF mice.
Conclusions:
- Porphyra yezoensis polysaccharides, particularly low molecular weight fractions like PYP4, demonstrate significant potential in mitigating vascular calcification.
- PYPs offer a protective effect against HAP-induced cellular damage and inhibit osteogenic differentiation, suggesting a therapeutic role in VC.
- PYP4 shows promise as a therapeutic agent for vascular calcification, addressing both cellular damage and osteoblast differentiation pathways.
Abstract:
Vascular calcification (VC) is a common pathological manifestation in patients with cardiovascular diseases, leading to high mortality in patients with chronic kidney diseases. The deposition of hydroxyapatite (HAP) crystals on vascular smooth muscle cells leads to cell damage, which promotes osteogenic transformation. In this study, four different molecular weights (MWs ) of Porphyra yezoensis polysaccharides (PYP1, PYP2, PYP3, and PYP4 with MWs of 576, 49.5, 12.6, and 4.02 kDa, respectively) were used to coat HAP, and the differences in toxicity and calcification of HAP on A7R5 cells before and after coating were studied. The results showed that PYPs could effectively reduce HAP damage to the A7R5 cells. Under the protection of PYPs, cell viability increased and lactate dehydrogenase release, active oxygen level, and cell necrosis rate decreased; also, the amount of the HAP crystals adhering to cell surfaces and entering cells decreased. PYPs with low molecular weights presented better protective effects than high-molecular-weight PYPs. PYPs also inhibited the osteogenic transformation of the A7R5 cells induced by HAP and decreased alkaline phosphatase (ALP) activity and expressions of bone/chondrocyte phenotype genes (runt-related factor 2, ALP, osteopontin, and osteocalcin). In the adenine-induced chronic renal failure (CRF) mouse VC model, PYP4 was found to obviously inhibit the aortic calcium level, and it also inhibited the serum creatinine, serum phosphorus and serum BUN levels. PYP4 (least molecular weight) showed the best inhibitory effect on calcification and may be considered as a candidate drug with therapeutic potential for inhibiting cellular damage and osteoblast differentiation induced by the HAP crystals.
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