Apoptosis of airway epithelial cells in response to meconium

Zagariya, Alexander; Bhat, Rama; Chari, Gopal; Uhal, Bruce D.; Navale, Shankararao; Vidyasagar, Dharmapuri

doi:10.1016/j.lfs.2004.10.033

Cited by 30 publications

(35 citation statements)

References 22 publications

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“…The apoptotic cells are identified by measuring caspase 3 expression. 28 Maximal expression of caspase 3 was also seen at 8 h after meconium instillation (Figure 1).…”

Section: Phospholipase Activationmentioning

confidence: 90%

“…Recent data from our laboratory indicate that captopril and inhibition of AT receptor action may diminish pulmonary epithelial apoptosis in meconium lungs. 28,37 Additional data from our laboratory show that cytokine-treated rabbit lung and human lung airway epithelial cell line A549 demonstrate a similar rate of lung apoptosis, compared to meconium-instilled lungs. 35,38 From the above discussion it may be postulated that intrapulmonary meconium induces influx of inflammatory cells in the lungs.…”

Section: Oxygen Radicals In Apoptosismentioning

confidence: 95%

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Studies of meconium-induced lung injury: inflammatory cytokine expression and apoptosis

Vidyasagar

Zagariya

2008

J Perinatol

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To review current literature related to cellular mechanisms of meconiuminduced lung injury (MILI). Review of published experimental in vitro and in vivo MAS studies using human and animal lung cells. We found that meconium induces expression of cytokines and angiotensin II (ANG II)-induced apoptotic process in the lung cells. We postulate that inflammatory cytokines induce ANG II expression, which causes apoptotic cell death after binding to its AT1 receptors. We also demonstrated expression of serpins associated with meconium instillation into the lungs. Serpins are proteins that inhibit cellular proteases and elastases. Expression of serpins may be an attempt to recover lung from these injurious effects. In summary our studies show that whereas meconium induces inflammatory cytokines and subsequent cell apoptosis, the lung cells also try to protect themselves by inducing serpins. The balance of these interactions will determine the residual damage. We believe these new findings are very important in understanding of MILI.

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“…The apoptotic cells are identified by measuring caspase 3 expression. 28 Maximal expression of caspase 3 was also seen at 8 h after meconium instillation (Figure 1).…”

Section: Phospholipase Activationmentioning

confidence: 90%

Section: Oxygen Radicals In Apoptosismentioning

confidence: 95%

Studies of meconium-induced lung injury: inflammatory cytokine expression and apoptosis

Vidyasagar

Zagariya

2008

J Perinatol

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“…66,67 Interest therefore was turned to the possibility that AECs dying in response to meconium might also require the local intrinsic RAS for their death and might be prevented from dying by ACE inhibitors of ANG receptor blockers. Several lines of investigation support the theory that meconium does indeed induce expression of the local RAS that might be amenable to pharmacologic blockade.…”

Section: The Endocrine Ras Versus Local Tissue Rasesmentioning

confidence: 99%

Angiotensin II in apoptotic lung injury: potential role in meconium aspiration syndrome

Uhal

Abdul-Hafez

2008

J Perinatol

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Meconium aspiration injures a number of cell types in the lung, most notably airway and alveolar epithelial lining cells. Recent data show that at least some of the cell death induced by meconium occurs by apoptosis, and therefore has the potential for pharmacologic inhibition through the use of apoptosis blockers or other strategies. Related work in adult animal models of lung injury has shown that apoptosis of lung epithelial cells induces a local (that is, entirely lung tissue specific) renin-angiotensin system (RAS L ). Furthermore, this inducible RAS L is required for the apoptotic response and affects other adjacent cell types through the release of angiotensin II and related peptides. This manuscript reviews the published data supporting this viewpoint as well as more recent works that suggest the involvement of a RAS L in the perinatal lung damage associated with meconium aspiration syndrome (MAS). The implications of these findings regarding their potential for the clinical management of MAS are also discussed.

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“…Furthermore, meconium-induced apoptosis may be inhibited by angiotensin-converting enzyme inhibitors, which may reduce injury. 18,19 Meconium is a potent complement activator and complement inhibition may represent a future therapeutic principle in MAS. 20 In the future all the principles discussed above may be combined to develop a powerful therapy for MAS.…”

Section: Discussionmentioning

confidence: 99%

Toxic effects of different meconium fractions on lung function: new therapeutic strategies for meconium aspiration syndrome?

et al. 2008

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To review and summarize experimental data examining the effects of different fractions of meconium, and to test the effect of albumin on meconium aspiration both as prophylactic and rescue treatment. Newborn piglets 2 to 5 days of age were made hypoxic and then instilled meconium or fractions of meconium intratracheally. Meconium-added albumin and albumin instilled after meconium were also tested. Lung function and inflammatory cytokines were measured. Both the lipid-and water-soluble fractions induce inflammation in the lungs with elevation of inflammatory cytokines. When meconium was mixed with albumin, the inflammatory effects of meconium were significantly ameliorated. Rescue therapy with intratracheal albumin 5 min after the meconium aspiration syndrome was induced also improved lung function. These results indicate that at least part of the symptoms seen in the meconium aspiration syndrome could be prevented by blocking the active substances of meconium such as bile acids and free fatty acids.

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Apoptosis of airway epithelial cells in response to meconium

Cited by 30 publications

References 22 publications

Studies of meconium-induced lung injury: inflammatory cytokine expression and apoptosis

Studies of meconium-induced lung injury: inflammatory cytokine expression and apoptosis

Angiotensin II in apoptotic lung injury: potential role in meconium aspiration syndrome

Toxic effects of different meconium fractions on lung function: new therapeutic strategies for meconium aspiration syndrome?

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