Chronic Inflammation Offers Hints About Viable Therapeutic Targets for Preeclampsia and Potentially Related Offspring Sequelae DOI Open Access
Jaya D. Prasad, Juliette Van Steenwinckel, Alistair J. Gunn

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(23), P. 12999 - 12999

Published: Dec. 3, 2024

The combination of hypertension with systemic inflammation during pregnancy is a hallmark preeclampsia, but both processes also convey dynamic information about its antecedents and correlates (e.g., fetal growth restriction) potentially related offspring sequelae. Causal inferences are further complicated by the increasingly frequent overlap restriction, multiple indicators acute chronic inflammation, decreased gestational length social vulnerability). This complexity prompted our group to summarize from mechanistic studies, integrated key clinical evidence, discuss possibility that sustained or intermittent inflammation-related phenomena offer hints viable therapeutic targets, not only for prevention neurobehavioral other developmental deficits appear be overrepresented in surviving offspring. Importantly, we feel carefully designed hypothesis-driven observational studies necessary if translate evidence into child health benefits, namely because disorders might contribute heightened risks neuroinflammation, arrested brain development, dysconnectivity survivors who exhibit problems later life.

Language: Английский

Prenatal inflammation exacerbates hyperoxia-induced neonatal brain injury DOI Creative Commons
Meray Serdar,

K. Walther,

Markus Gallert

et al.

Journal of Neuroinflammation, Journal Year: 2025, Volume and Issue: 22(1)

Published: Feb. 28, 2025

Abstract Background Premature born infants are at high risk to develop white matter injury (WMI). Hyperoxia and perinatal inflammation main factors for preterm birth associated brain injury. To date the majority of experimental studies have focused on isolated insults. However, clinically, WMI is a multifactorial disorder caused by variety triggers. establish clinically relevant rodent model WMI, we combined prenatal with postnatal hyperoxia investigate individual, additive or synergistic effects inflammatory processes, myelination grey development. Methods At embryonic day 20, pregnant Wistar rat dams received either single intraperitoneal injection 100 µg/ kg lipopolysaccharide (LPS) sodium chloride. Offspring were exposed (80% O 2 ) normoxia (21% from 3 5. Animals sacrificed immediately after 6 days later, corresponding term-equivalent age. White development neuroinflammatory responses investigated cellular molecular levels applying immunohistochemistry, western blotting, real time PCR in tissues multiplex protein expression analysis serum samples. Results Prenatal resulted reduced body weight length offspring, accompanied increased leptin term equivalent The altered parameters, like weight, decreased volume, thinning deep cortical layers hypomyelination. As potential underlying mechanisms, identified severe deficits an microglia activation elevated cytokine tissues, while peripheral reduced. Interestingly, size mainly mediated LPS, independent hyperoxia, oligodendrocyte degeneration was induced inflammation. pathological changes, including size, deficits, expression, detected. Conclusion results aggravated compared insults, making it ideal improve our understanding complex pathophysiology evaluate urgently needed therapies.

Language: Английский

Citations

0
Targeting Neuroinflammation in Preterm White Matter Injury: Therapeutic Potential of Mesenchymal Stem Cell-Derived Exosomes DOI Creative Commons
Xinling Zhang, Yuhang Zhang,

Xirui Peng

et al.

Cellular and Molecular Neurobiology, Journal Year: 2025, Volume and Issue: 45(1)

Published: March 12, 2025

Neuroinflammation is a key factor in the development of preterm white matter injury (PWMI), leading to glial cell dysfunction, arrest oligodendrocyte maturation, and long-term neurological damage. As potential therapeutic strategy, mesenchymal stem cells (MSCs) exhibit significant immunomodulatory regenerative potential. Recent studies suggest that primary mechanism MSC action their paracrine effects, particularly mediated by extracellular vesicles, with MSC-derived exosomes (MSC-Exos) being mediators. MSC-Exos, enriched lipids, proteins, nucleic acids, regulate neuroinflammation modulating activity influencing signaling pathways associated inflammation repair. Preclinical evidence has indicated MSC-Exos can suppress activation microglia astrocytes, promote enhance myelination, highlighting as cell-free treatment for PWMI. However, there are paucity comprehensive reviews on how PWMI through specific pathways. This review aims summarize which modulate discuss challenges clinical application MSC-Exos-based therapies.

Language: Английский

Citations

0
Excitotoxic lesion in the corpus callosum of neonatal rats: A model for encephalopathy of prematurity DOI

Rafael Arrazola,

Araceli Espinosa‐Jeffrey, Norma Serafín

et al.

Neuroscience, Journal Year: 2025, Volume and Issue: unknown

Published: March 1, 2025

Language: Английский

Citations

0
Human milk oligosaccharides improve white matter and interneuron development in a double-hit rat model for preterm brain injury DOI
Myrna J. V. Brandt, Juliette Van Steenwinckel,

Bobbie-Louise Van Emst

et al.

Neuropharmacology, Journal Year: 2025, Volume and Issue: unknown, P. 110507 - 110507

Published: May 1, 2025

Language: Английский

Citations

0
Chronic Inflammation Offers Hints About Viable Therapeutic Targets for Preeclampsia and Potentially Related Offspring Sequelae DOI Open Access
Jaya D. Prasad, Juliette Van Steenwinckel, Alistair J. Gunn

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(23), P. 12999 - 12999

Published: Dec. 3, 2024

The combination of hypertension with systemic inflammation during pregnancy is a hallmark preeclampsia, but both processes also convey dynamic information about its antecedents and correlates (e.g., fetal growth restriction) potentially related offspring sequelae. Causal inferences are further complicated by the increasingly frequent overlap restriction, multiple indicators acute chronic inflammation, decreased gestational length social vulnerability). This complexity prompted our group to summarize from mechanistic studies, integrated key clinical evidence, discuss possibility that sustained or intermittent inflammation-related phenomena offer hints viable therapeutic targets, not only for prevention neurobehavioral other developmental deficits appear be overrepresented in surviving offspring. Importantly, we feel carefully designed hypothesis-driven observational studies necessary if translate evidence into child health benefits, namely because disorders might contribute heightened risks neuroinflammation, arrested brain development, dysconnectivity survivors who exhibit problems later life.

Language: Английский

Citations

0