Silica nanoparticles induce pulmonary damage in rats via VEGFC/D–VEGFR3 signaling-mediated lymphangiogenesis and remodeling

Silica nanoparticles (SiNPs) are widely used as drug carriers for improving drug delivery and retention. The lungs are highly sensitive to the toxicity of SiNPs entering the respiratory tract. Furthermore, pulmonary lymphangiogenesis, which is the growth of lymphatic vessels observed during multiple...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Yu, Yanan [verfasserIn] Pan, Yujie [verfasserIn] Chang, Bing [verfasserIn] Zhao, Xiaoxu [verfasserIn] Qu, Kunlong [verfasserIn] Song, Yuguo [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	Nano-silica Inflammation-associated lymphangiogenesis Lymphatic vessel remodelling Pulmonary permeability Lymphatic endothelial cell damage

Übergeordnetes Werk:	Enthalten in: Toxicology - Amsterdam [u.a.] : Elsevier Science, 1973, 493
Übergeordnetes Werk:	volume:493

DOI / URN:	10.1016/j.tox.2023.153552

Katalog-ID:	ELV010398457

Internformat


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245	1	0	\|a Silica nanoparticles induce pulmonary damage in rats via VEGFC/D–VEGFR3 signaling-mediated lymphangiogenesis and remodeling
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520			\|a Silica nanoparticles (SiNPs) are widely used as drug carriers for improving drug delivery and retention. The lungs are highly sensitive to the toxicity of SiNPs entering the respiratory tract. Furthermore, pulmonary lymphangiogenesis, which is the growth of lymphatic vessels observed during multiple pulmonary diseases, plays a vital role in promoting the lymphatic transport of silica in the lungs. However, more research is required on the effects of SiNPs on pulmonary lymphangiogenesis. We investigated the effect of SiNP-induced pulmonary toxicity on lymphatic vessel formation in rats and evaluated the toxicity and possible molecular mechanisms of 20-nm SiNPs. Saline containing 3.0, 6.0, and 12.0 mg/kg of SiNPs was instilled intrathecally into female Wistar rats once a day for five days, then sacrificed on day seven. Lung histopathology, pulmonary permeability, pulmonary lymphatic vessel density changes, and the ultrastructure of the lymph trunk were investigated using light microscopy, spectrophotometry, immunofluorescence, and transmission electron microscopy. CD45 expression in lung tissues was determined using immunohistochemical staining, and protein expression in the lung and lymph trunk was quantified using western blotting. We observed increased pulmonary inflammation and permeability, lymphatic endothelial cell damage, pulmonary lymphangiogenesis, and remodeling with increasing SiNP concentration. Moreover, SiNPs activated the VEGFC/D–VEGFR3 signaling pathway in the lung and lymphatic vessel tissues. SiNPs caused pulmonary damage, increased permeability and resulted in inflammation-associated lymphangiogenesis and remodeling by activating VEGFC/D–VEGFR3 signaling. Our findings provide evidence for SiNP-induced pulmonary damage and a new perspective for the prevention and treatment of occupational exposure to SiNPs.
650		4	\|a Nano-silica
650		4	\|a Inflammation-associated lymphangiogenesis
650		4	\|a Lymphatic vessel remodelling
650		4	\|a Pulmonary permeability
650		4	\|a Lymphatic endothelial cell damage
700	1		\|a Pan, Yujie \|e verfasserin \|4 aut
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700	1		\|a Qu, Kunlong \|e verfasserin \|4 aut
700	1		\|a Song, Yuguo \|e verfasserin \|4 aut
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allfields	10.1016/j.tox.2023.153552 doi (DE-627)ELV010398457 (ELSEVIER)S0300-483X(23)00138-5 DE-627 ger DE-627 rda eng 570 540 610 VZ 44.39 bkl Yu, Yanan verfasserin aut Silica nanoparticles induce pulmonary damage in rats via VEGFC/D–VEGFR3 signaling-mediated lymphangiogenesis and remodeling 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Silica nanoparticles (SiNPs) are widely used as drug carriers for improving drug delivery and retention. The lungs are highly sensitive to the toxicity of SiNPs entering the respiratory tract. Furthermore, pulmonary lymphangiogenesis, which is the growth of lymphatic vessels observed during multiple pulmonary diseases, plays a vital role in promoting the lymphatic transport of silica in the lungs. However, more research is required on the effects of SiNPs on pulmonary lymphangiogenesis. We investigated the effect of SiNP-induced pulmonary toxicity on lymphatic vessel formation in rats and evaluated the toxicity and possible molecular mechanisms of 20-nm SiNPs. Saline containing 3.0, 6.0, and 12.0 mg/kg of SiNPs was instilled intrathecally into female Wistar rats once a day for five days, then sacrificed on day seven. Lung histopathology, pulmonary permeability, pulmonary lymphatic vessel density changes, and the ultrastructure of the lymph trunk were investigated using light microscopy, spectrophotometry, immunofluorescence, and transmission electron microscopy. CD45 expression in lung tissues was determined using immunohistochemical staining, and protein expression in the lung and lymph trunk was quantified using western blotting. We observed increased pulmonary inflammation and permeability, lymphatic endothelial cell damage, pulmonary lymphangiogenesis, and remodeling with increasing SiNP concentration. Moreover, SiNPs activated the VEGFC/D–VEGFR3 signaling pathway in the lung and lymphatic vessel tissues. SiNPs caused pulmonary damage, increased permeability and resulted in inflammation-associated lymphangiogenesis and remodeling by activating VEGFC/D–VEGFR3 signaling. Our findings provide evidence for SiNP-induced pulmonary damage and a new perspective for the prevention and treatment of occupational exposure to SiNPs. Nano-silica Inflammation-associated lymphangiogenesis Lymphatic vessel remodelling Pulmonary permeability Lymphatic endothelial cell damage Pan, Yujie verfasserin aut Chang, Bing verfasserin aut Zhao, Xiaoxu verfasserin aut Qu, Kunlong verfasserin aut Song, Yuguo verfasserin aut Enthalten in Toxicology Amsterdam [u.a.] : Elsevier Science, 1973 493 Online-Ressource (DE-627)306710838 (DE-600)1500781-9 (DE-576)082436053 1879-3185 nnns volume:493 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.39 Toxikologie VZ AR 493
spelling	10.1016/j.tox.2023.153552 doi (DE-627)ELV010398457 (ELSEVIER)S0300-483X(23)00138-5 DE-627 ger DE-627 rda eng 570 540 610 VZ 44.39 bkl Yu, Yanan verfasserin aut Silica nanoparticles induce pulmonary damage in rats via VEGFC/D–VEGFR3 signaling-mediated lymphangiogenesis and remodeling 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Silica nanoparticles (SiNPs) are widely used as drug carriers for improving drug delivery and retention. The lungs are highly sensitive to the toxicity of SiNPs entering the respiratory tract. Furthermore, pulmonary lymphangiogenesis, which is the growth of lymphatic vessels observed during multiple pulmonary diseases, plays a vital role in promoting the lymphatic transport of silica in the lungs. However, more research is required on the effects of SiNPs on pulmonary lymphangiogenesis. We investigated the effect of SiNP-induced pulmonary toxicity on lymphatic vessel formation in rats and evaluated the toxicity and possible molecular mechanisms of 20-nm SiNPs. Saline containing 3.0, 6.0, and 12.0 mg/kg of SiNPs was instilled intrathecally into female Wistar rats once a day for five days, then sacrificed on day seven. Lung histopathology, pulmonary permeability, pulmonary lymphatic vessel density changes, and the ultrastructure of the lymph trunk were investigated using light microscopy, spectrophotometry, immunofluorescence, and transmission electron microscopy. CD45 expression in lung tissues was determined using immunohistochemical staining, and protein expression in the lung and lymph trunk was quantified using western blotting. We observed increased pulmonary inflammation and permeability, lymphatic endothelial cell damage, pulmonary lymphangiogenesis, and remodeling with increasing SiNP concentration. Moreover, SiNPs activated the VEGFC/D–VEGFR3 signaling pathway in the lung and lymphatic vessel tissues. SiNPs caused pulmonary damage, increased permeability and resulted in inflammation-associated lymphangiogenesis and remodeling by activating VEGFC/D–VEGFR3 signaling. Our findings provide evidence for SiNP-induced pulmonary damage and a new perspective for the prevention and treatment of occupational exposure to SiNPs. Nano-silica Inflammation-associated lymphangiogenesis Lymphatic vessel remodelling Pulmonary permeability Lymphatic endothelial cell damage Pan, Yujie verfasserin aut Chang, Bing verfasserin aut Zhao, Xiaoxu verfasserin aut Qu, Kunlong verfasserin aut Song, Yuguo verfasserin aut Enthalten in Toxicology Amsterdam [u.a.] : Elsevier Science, 1973 493 Online-Ressource (DE-627)306710838 (DE-600)1500781-9 (DE-576)082436053 1879-3185 nnns volume:493 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.39 Toxikologie VZ AR 493
allfields_unstemmed	10.1016/j.tox.2023.153552 doi (DE-627)ELV010398457 (ELSEVIER)S0300-483X(23)00138-5 DE-627 ger DE-627 rda eng 570 540 610 VZ 44.39 bkl Yu, Yanan verfasserin aut Silica nanoparticles induce pulmonary damage in rats via VEGFC/D–VEGFR3 signaling-mediated lymphangiogenesis and remodeling 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Silica nanoparticles (SiNPs) are widely used as drug carriers for improving drug delivery and retention. The lungs are highly sensitive to the toxicity of SiNPs entering the respiratory tract. Furthermore, pulmonary lymphangiogenesis, which is the growth of lymphatic vessels observed during multiple pulmonary diseases, plays a vital role in promoting the lymphatic transport of silica in the lungs. However, more research is required on the effects of SiNPs on pulmonary lymphangiogenesis. We investigated the effect of SiNP-induced pulmonary toxicity on lymphatic vessel formation in rats and evaluated the toxicity and possible molecular mechanisms of 20-nm SiNPs. Saline containing 3.0, 6.0, and 12.0 mg/kg of SiNPs was instilled intrathecally into female Wistar rats once a day for five days, then sacrificed on day seven. Lung histopathology, pulmonary permeability, pulmonary lymphatic vessel density changes, and the ultrastructure of the lymph trunk were investigated using light microscopy, spectrophotometry, immunofluorescence, and transmission electron microscopy. CD45 expression in lung tissues was determined using immunohistochemical staining, and protein expression in the lung and lymph trunk was quantified using western blotting. We observed increased pulmonary inflammation and permeability, lymphatic endothelial cell damage, pulmonary lymphangiogenesis, and remodeling with increasing SiNP concentration. Moreover, SiNPs activated the VEGFC/D–VEGFR3 signaling pathway in the lung and lymphatic vessel tissues. SiNPs caused pulmonary damage, increased permeability and resulted in inflammation-associated lymphangiogenesis and remodeling by activating VEGFC/D–VEGFR3 signaling. Our findings provide evidence for SiNP-induced pulmonary damage and a new perspective for the prevention and treatment of occupational exposure to SiNPs. Nano-silica Inflammation-associated lymphangiogenesis Lymphatic vessel remodelling Pulmonary permeability Lymphatic endothelial cell damage Pan, Yujie verfasserin aut Chang, Bing verfasserin aut Zhao, Xiaoxu verfasserin aut Qu, Kunlong verfasserin aut Song, Yuguo verfasserin aut Enthalten in Toxicology Amsterdam [u.a.] : Elsevier Science, 1973 493 Online-Ressource (DE-627)306710838 (DE-600)1500781-9 (DE-576)082436053 1879-3185 nnns volume:493 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.39 Toxikologie VZ AR 493
allfieldsGer	10.1016/j.tox.2023.153552 doi (DE-627)ELV010398457 (ELSEVIER)S0300-483X(23)00138-5 DE-627 ger DE-627 rda eng 570 540 610 VZ 44.39 bkl Yu, Yanan verfasserin aut Silica nanoparticles induce pulmonary damage in rats via VEGFC/D–VEGFR3 signaling-mediated lymphangiogenesis and remodeling 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Silica nanoparticles (SiNPs) are widely used as drug carriers for improving drug delivery and retention. The lungs are highly sensitive to the toxicity of SiNPs entering the respiratory tract. Furthermore, pulmonary lymphangiogenesis, which is the growth of lymphatic vessels observed during multiple pulmonary diseases, plays a vital role in promoting the lymphatic transport of silica in the lungs. However, more research is required on the effects of SiNPs on pulmonary lymphangiogenesis. We investigated the effect of SiNP-induced pulmonary toxicity on lymphatic vessel formation in rats and evaluated the toxicity and possible molecular mechanisms of 20-nm SiNPs. Saline containing 3.0, 6.0, and 12.0 mg/kg of SiNPs was instilled intrathecally into female Wistar rats once a day for five days, then sacrificed on day seven. Lung histopathology, pulmonary permeability, pulmonary lymphatic vessel density changes, and the ultrastructure of the lymph trunk were investigated using light microscopy, spectrophotometry, immunofluorescence, and transmission electron microscopy. CD45 expression in lung tissues was determined using immunohistochemical staining, and protein expression in the lung and lymph trunk was quantified using western blotting. We observed increased pulmonary inflammation and permeability, lymphatic endothelial cell damage, pulmonary lymphangiogenesis, and remodeling with increasing SiNP concentration. Moreover, SiNPs activated the VEGFC/D–VEGFR3 signaling pathway in the lung and lymphatic vessel tissues. SiNPs caused pulmonary damage, increased permeability and resulted in inflammation-associated lymphangiogenesis and remodeling by activating VEGFC/D–VEGFR3 signaling. Our findings provide evidence for SiNP-induced pulmonary damage and a new perspective for the prevention and treatment of occupational exposure to SiNPs. Nano-silica Inflammation-associated lymphangiogenesis Lymphatic vessel remodelling Pulmonary permeability Lymphatic endothelial cell damage Pan, Yujie verfasserin aut Chang, Bing verfasserin aut Zhao, Xiaoxu verfasserin aut Qu, Kunlong verfasserin aut Song, Yuguo verfasserin aut Enthalten in Toxicology Amsterdam [u.a.] : Elsevier Science, 1973 493 Online-Ressource (DE-627)306710838 (DE-600)1500781-9 (DE-576)082436053 1879-3185 nnns volume:493 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.39 Toxikologie VZ AR 493
allfieldsSound	10.1016/j.tox.2023.153552 doi (DE-627)ELV010398457 (ELSEVIER)S0300-483X(23)00138-5 DE-627 ger DE-627 rda eng 570 540 610 VZ 44.39 bkl Yu, Yanan verfasserin aut Silica nanoparticles induce pulmonary damage in rats via VEGFC/D–VEGFR3 signaling-mediated lymphangiogenesis and remodeling 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Silica nanoparticles (SiNPs) are widely used as drug carriers for improving drug delivery and retention. The lungs are highly sensitive to the toxicity of SiNPs entering the respiratory tract. Furthermore, pulmonary lymphangiogenesis, which is the growth of lymphatic vessels observed during multiple pulmonary diseases, plays a vital role in promoting the lymphatic transport of silica in the lungs. However, more research is required on the effects of SiNPs on pulmonary lymphangiogenesis. We investigated the effect of SiNP-induced pulmonary toxicity on lymphatic vessel formation in rats and evaluated the toxicity and possible molecular mechanisms of 20-nm SiNPs. Saline containing 3.0, 6.0, and 12.0 mg/kg of SiNPs was instilled intrathecally into female Wistar rats once a day for five days, then sacrificed on day seven. Lung histopathology, pulmonary permeability, pulmonary lymphatic vessel density changes, and the ultrastructure of the lymph trunk were investigated using light microscopy, spectrophotometry, immunofluorescence, and transmission electron microscopy. CD45 expression in lung tissues was determined using immunohistochemical staining, and protein expression in the lung and lymph trunk was quantified using western blotting. We observed increased pulmonary inflammation and permeability, lymphatic endothelial cell damage, pulmonary lymphangiogenesis, and remodeling with increasing SiNP concentration. Moreover, SiNPs activated the VEGFC/D–VEGFR3 signaling pathway in the lung and lymphatic vessel tissues. SiNPs caused pulmonary damage, increased permeability and resulted in inflammation-associated lymphangiogenesis and remodeling by activating VEGFC/D–VEGFR3 signaling. Our findings provide evidence for SiNP-induced pulmonary damage and a new perspective for the prevention and treatment of occupational exposure to SiNPs. Nano-silica Inflammation-associated lymphangiogenesis Lymphatic vessel remodelling Pulmonary permeability Lymphatic endothelial cell damage Pan, Yujie verfasserin aut Chang, Bing verfasserin aut Zhao, Xiaoxu verfasserin aut Qu, Kunlong verfasserin aut Song, Yuguo verfasserin aut Enthalten in Toxicology Amsterdam [u.a.] : Elsevier Science, 1973 493 Online-Ressource (DE-627)306710838 (DE-600)1500781-9 (DE-576)082436053 1879-3185 nnns volume:493 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.39 Toxikologie VZ AR 493
language	English
source	Enthalten in Toxicology 493 volume:493
sourceStr	Enthalten in Toxicology 493 volume:493
format_phy_str_mv	Article
bklname	Toxikologie
institution	findex.gbv.de
topic_facet	Nano-silica Inflammation-associated lymphangiogenesis Lymphatic vessel remodelling Pulmonary permeability Lymphatic endothelial cell damage
dewey-raw	570
isfreeaccess_bool	false
container_title	Toxicology
authorswithroles_txt_mv	Yu, Yanan @@aut@@ Pan, Yujie @@aut@@ Chang, Bing @@aut@@ Zhao, Xiaoxu @@aut@@ Qu, Kunlong @@aut@@ Song, Yuguo @@aut@@
publishDateDaySort_date	2023-01-01T00:00:00Z
hierarchy_top_id	306710838
dewey-sort	3570
id	ELV010398457
language_de	englisch
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author	Yu, Yanan
spellingShingle	Yu, Yanan ddc 570 bkl 44.39 misc Nano-silica misc Inflammation-associated lymphangiogenesis misc Lymphatic vessel remodelling misc Pulmonary permeability misc Lymphatic endothelial cell damage Silica nanoparticles induce pulmonary damage in rats via VEGFC/D–VEGFR3 signaling-mediated lymphangiogenesis and remodeling
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topic_title	570 540 610 VZ 44.39 bkl Silica nanoparticles induce pulmonary damage in rats via VEGFC/D–VEGFR3 signaling-mediated lymphangiogenesis and remodeling Nano-silica Inflammation-associated lymphangiogenesis Lymphatic vessel remodelling Pulmonary permeability Lymphatic endothelial cell damage
topic	ddc 570 bkl 44.39 misc Nano-silica misc Inflammation-associated lymphangiogenesis misc Lymphatic vessel remodelling misc Pulmonary permeability misc Lymphatic endothelial cell damage
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title	Silica nanoparticles induce pulmonary damage in rats via VEGFC/D–VEGFR3 signaling-mediated lymphangiogenesis and remodeling
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title_full	Silica nanoparticles induce pulmonary damage in rats via VEGFC/D–VEGFR3 signaling-mediated lymphangiogenesis and remodeling
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title_sort	silica nanoparticles induce pulmonary damage in rats via vegfc/d–vegfr3 signaling-mediated lymphangiogenesis and remodeling
title_auth	Silica nanoparticles induce pulmonary damage in rats via VEGFC/D–VEGFR3 signaling-mediated lymphangiogenesis and remodeling
abstract	Silica nanoparticles (SiNPs) are widely used as drug carriers for improving drug delivery and retention. The lungs are highly sensitive to the toxicity of SiNPs entering the respiratory tract. Furthermore, pulmonary lymphangiogenesis, which is the growth of lymphatic vessels observed during multiple pulmonary diseases, plays a vital role in promoting the lymphatic transport of silica in the lungs. However, more research is required on the effects of SiNPs on pulmonary lymphangiogenesis. We investigated the effect of SiNP-induced pulmonary toxicity on lymphatic vessel formation in rats and evaluated the toxicity and possible molecular mechanisms of 20-nm SiNPs. Saline containing 3.0, 6.0, and 12.0 mg/kg of SiNPs was instilled intrathecally into female Wistar rats once a day for five days, then sacrificed on day seven. Lung histopathology, pulmonary permeability, pulmonary lymphatic vessel density changes, and the ultrastructure of the lymph trunk were investigated using light microscopy, spectrophotometry, immunofluorescence, and transmission electron microscopy. CD45 expression in lung tissues was determined using immunohistochemical staining, and protein expression in the lung and lymph trunk was quantified using western blotting. We observed increased pulmonary inflammation and permeability, lymphatic endothelial cell damage, pulmonary lymphangiogenesis, and remodeling with increasing SiNP concentration. Moreover, SiNPs activated the VEGFC/D–VEGFR3 signaling pathway in the lung and lymphatic vessel tissues. SiNPs caused pulmonary damage, increased permeability and resulted in inflammation-associated lymphangiogenesis and remodeling by activating VEGFC/D–VEGFR3 signaling. Our findings provide evidence for SiNP-induced pulmonary damage and a new perspective for the prevention and treatment of occupational exposure to SiNPs.
abstractGer	Silica nanoparticles (SiNPs) are widely used as drug carriers for improving drug delivery and retention. The lungs are highly sensitive to the toxicity of SiNPs entering the respiratory tract. Furthermore, pulmonary lymphangiogenesis, which is the growth of lymphatic vessels observed during multiple pulmonary diseases, plays a vital role in promoting the lymphatic transport of silica in the lungs. However, more research is required on the effects of SiNPs on pulmonary lymphangiogenesis. We investigated the effect of SiNP-induced pulmonary toxicity on lymphatic vessel formation in rats and evaluated the toxicity and possible molecular mechanisms of 20-nm SiNPs. Saline containing 3.0, 6.0, and 12.0 mg/kg of SiNPs was instilled intrathecally into female Wistar rats once a day for five days, then sacrificed on day seven. Lung histopathology, pulmonary permeability, pulmonary lymphatic vessel density changes, and the ultrastructure of the lymph trunk were investigated using light microscopy, spectrophotometry, immunofluorescence, and transmission electron microscopy. CD45 expression in lung tissues was determined using immunohistochemical staining, and protein expression in the lung and lymph trunk was quantified using western blotting. We observed increased pulmonary inflammation and permeability, lymphatic endothelial cell damage, pulmonary lymphangiogenesis, and remodeling with increasing SiNP concentration. Moreover, SiNPs activated the VEGFC/D–VEGFR3 signaling pathway in the lung and lymphatic vessel tissues. SiNPs caused pulmonary damage, increased permeability and resulted in inflammation-associated lymphangiogenesis and remodeling by activating VEGFC/D–VEGFR3 signaling. Our findings provide evidence for SiNP-induced pulmonary damage and a new perspective for the prevention and treatment of occupational exposure to SiNPs.
abstract_unstemmed	Silica nanoparticles (SiNPs) are widely used as drug carriers for improving drug delivery and retention. The lungs are highly sensitive to the toxicity of SiNPs entering the respiratory tract. Furthermore, pulmonary lymphangiogenesis, which is the growth of lymphatic vessels observed during multiple pulmonary diseases, plays a vital role in promoting the lymphatic transport of silica in the lungs. However, more research is required on the effects of SiNPs on pulmonary lymphangiogenesis. We investigated the effect of SiNP-induced pulmonary toxicity on lymphatic vessel formation in rats and evaluated the toxicity and possible molecular mechanisms of 20-nm SiNPs. Saline containing 3.0, 6.0, and 12.0 mg/kg of SiNPs was instilled intrathecally into female Wistar rats once a day for five days, then sacrificed on day seven. Lung histopathology, pulmonary permeability, pulmonary lymphatic vessel density changes, and the ultrastructure of the lymph trunk were investigated using light microscopy, spectrophotometry, immunofluorescence, and transmission electron microscopy. CD45 expression in lung tissues was determined using immunohistochemical staining, and protein expression in the lung and lymph trunk was quantified using western blotting. We observed increased pulmonary inflammation and permeability, lymphatic endothelial cell damage, pulmonary lymphangiogenesis, and remodeling with increasing SiNP concentration. Moreover, SiNPs activated the VEGFC/D–VEGFR3 signaling pathway in the lung and lymphatic vessel tissues. SiNPs caused pulmonary damage, increased permeability and resulted in inflammation-associated lymphangiogenesis and remodeling by activating VEGFC/D–VEGFR3 signaling. Our findings provide evidence for SiNP-induced pulmonary damage and a new perspective for the prevention and treatment of occupational exposure to SiNPs.
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title_short	Silica nanoparticles induce pulmonary damage in rats via VEGFC/D–VEGFR3 signaling-mediated lymphangiogenesis and remodeling
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author2	Pan, Yujie Chang, Bing Zhao, Xiaoxu Qu, Kunlong Song, Yuguo
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up_date	2024-07-06T17:51:05.003Z
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Silica nanoparticles induce pulmonary damage in rats via VEGFC/D–VEGFR3 signaling-mediated lymphangiogenesis and remodeling

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