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From the cord to the clinic: What my newborn reminded me about wound healing

It’s 2am. The baby is awake. And naturally, my mind has landed on proteomics.

It’s 2am. Our son Freddie is six weeks old, approximately the size of a large watermelon (he was 4.32kg at birth already), and has opinions about sleep that are, frankly, difficult to respect. I’m letting my lovely wife sleep while I’m pacing the passage in the dark, doing the rhythmic sway that seems to be the only reliable tool in the parenting arsenal. My brain, refusing to switch off, has somehow wandered back to the stack of cord blood banking brochures we got before Freddie was born.

 

We made our decision about cord blood banking before he arrived. We’d read the materials carefully, talked it through, weighed the options. But there’s something about a dozing (well, almost dozing) newborn in your arms that makes you think about biology differently. About what this small person is made of. About what was in that cord, and where it might go.

 

And then, as tends to happen with me at 2am, I started thinking about the research.

So, what exactly is cord blood banking?

When a baby is born, the umbilical cord that has been the lifeline between mother and child for nine months is clamped and cut. What most people don’t realise is that the blood remaining in that cord (and the cord itself) is extraordinarily rich in stem cells and biological compounds that have powerful regenerative potential.

 

Cord blood banking is the process of collecting and storing this blood for potential future medical use. Think of it as a kind of biological insurance policy: a personal reserve of your child’s stem cells that could, one day, be used to treat blood cancers, immune disorders, and a growing number of other conditions. Collection happens immediately after birth (painless for both mother and baby) and the blood is then processed, tested, and cryogenically frozen at temperatures below -150°C, where it can remain viable for decades.

 

In South Africa, cord blood banking is offered through private companies, most notably Next Biosciences, a Midrand-based company that has been at the forefront of cellular therapy and cord tissue products on the continent. Families can choose to privately bank their baby’s cord blood (reserved for the family’s own future use) or donate to a public bank, where it becomes available for research and transplantation for others in need.

 

But here’s the thing that gets me, pacing the passage at 2am: the biological value in cord blood isn’t only about stem cells. The serum (the liquid component of the blood) is packed with growth factors, cytokines, and chemokines: molecular messengers that instruct cells to proliferate, migrate, reduce inflammation, and rebuild tissue. Which brings me, rather neatly, to the research I want to tell you about.

The problem with diabetic wounds

Diabetes is one of the most significant global health crises of our time. By 2030, over 140 million people in developing countries are expected to be living with the disease and its complications. One of the most debilitating and least discussed of those complications is chronic wound formation. Diabetic wounds affect between 4 and 10% of people living with diabetes, with a lifetime risk as high as 25%, and the global annual cost of treating them exceeds $13 billion USD. In South Africa specifically, diabetes-related amputations in the public healthcare sector have risen sharply over the past decade, accounting for around 80% of all non-traumatic amputations.

 

The cruel irony of a diabetic wound is that the very environment that causes it also prevents it from healing. High blood sugar, chronic inflammation, oxidative stress, and poor circulation all disrupt the wound microenvironment at a cellular and molecular level. Standard treatments (debridement, pressure offloading, infection management) help, but they don’t address the underlying biochemical chaos. Wounds can take between 12 and 62 weeks to heal, and recur at rates of up to 80%. For many patients in lower-income settings, the endpoint is amputation.

 

So the question our research team set out to answer was: Can we do better? Specifically, can combining two biological products, namely cord blood serum and amniotic membrane, create a treatment greater than the sum of its parts?

Two products, one hypothesis

The first product was umbilical cord blood serum, or UCBS - yes, derived from cord blood donations, supplied by Next Biosciences. Our multiplex analysis of 14 different donor samples confirmed what the literature already suggested: this is a potent biological cocktail. The standout molecules included SCGFb (stem cell growth factor beta) at concentrations approaching 47,000 pg/mL, HGF (hepatocyte growth factor) at over 1,000 pg/mL, and MIF, a chemokine that helps coordinate the immune response. These aren’t trace amounts. This material is genuinely, measurably biologically active.

 

The second product was a decellularised amniotic membrane - essentially, the inner lining of the placenta, processed to remove cells while preserving its collagen-rich scaffold structure. Amniotic membrane is rich in collagen types IV, V, and VII, growth factors, and protease inhibitors. Applied to a wound, it provides a physical framework for cell attachment and tissue regeneration. Randomised controlled trials have already shown that amniotic membrane products reduce healing times in diabetic wounds compared to standard care alone, but around 20% of wounds still don’t close within 12 weeks, and recurrence rates remain significant.

 

The hypothesis was elegant: apply cord blood serum first to prime the wound bed’s regenerative response during the early post-injury window, then layer on the amniotic membrane scaffold a few days later to give cells something to build on. A biochemical one-two punch: first the signal, then the scaffold.

The experiment

We worked with 23 obese, diabetic mice: a model called ob/ob, animals that are severely obese and have confirmed type 2 diabetes with blood glucose levels well above the normal range. Full-thickness skin wounds were created on their backs, and the animals were divided into four groups: a control group receiving standard wound dressing only; a group receiving cord blood serum on day 0; a group receiving the amniotic membrane on day 0; and a combined group receiving cord blood serum on day 0, followed by the amniotic membrane applied on day 3. Wounds were photographed and measured at days 0, 3, 7, 10, and 14. At endpoint, tissue was harvested for histological analysis (examining stained tissue sections under the microscope) and for proteomics. The proteomic piece is where I came in.

Healers, non-healers, and a plot twist

Here’s where things got interesting, and more complicated than we’d hoped. In every treatment group, approximately half the wounds responded well to treatment, and half did not. The non-healing wounds developed wet, excessive slough; that yellowish, unpleasant tissue familiar to anyone who has managed a wound that refuses to progress, and under the microscope showed what appeared to be bacterial aggregates and biofilm formation. Crucially, none of the untreated control wounds showed any signs of infection. This was a signal we couldn’t set aside: the biological treatments helping some wounds appeared to be creating conditions that worsened others.

 

Among the healers, though, the combined treatment group showed the most impressive results; not just at the surface, but in the depth of tissue repair. All healer groups achieved near-complete re-epithelisation, meaning the skin surface regrew across the wound. But only the combined treatment group showed full regeneration of the underlying layers: an intact dermis, collagen deposition, reformation of dermal white adipose tissue, regrowth of skin appendages such as hair follicles and glands, and even repair of the muscular layer beneath the skin. The wound area was, histologically, nearly indistinguishable from uninjured skin. The combined group’s histology score was 9.2 out of a possible 12, compared to 5.4 for the untreated control, and the amniotic membrane alone scored 8.2. The cord blood serum alone, interestingly, didn’t significantly outperform the control on histology — suggesting that its real power is as a primer for something else to follow.

 

This distinction matters enormously in clinical terms. Superficial wound closure is one thing, but if the underlying tissue hasn’t properly regenerated, the wound is primed to recur. What the combined treatment appeared to offer was not just closure, but resolution.

The molecular picture

At the endpoint, we performed a deep proteomic analysis of wound tissue: identifying and quantifying the proteins present in wounds on day 14. In total, we catalogued 4,494 proteins and 13,833 peptides across samples. Modern mass spectrometry is a remarkable thing.

 

The results told a coherent story. In the UCBS + amniotic membrane healer wounds, the vast majority of proteins detected were downregulated relative to untreated controls. What this tells us is that the combined treatment group had, in molecular terms, largely finished healing; the inflammatory and metabolic processes that drive wound activity had quietened down. The untreated control wounds, by contrast, were still biochemically active on day 14: metabolic pathways, catabolic processes, and inflammatory signalling cascades all still running. The wound hadn’t resolved; it was still in the process of trying.

 

Among the 37 proteins confirmed as significantly differentially expressed, those downregulated in the treatment group were involved in lipid metabolism, fatty acid oxidation, the TCA cycle, and TNF-alpha–associated NF-kB signalling - a major inflammatory pathway. Together, these findings suggested that the combined treatment hadn’t just helped the wounds close; it had helped them reach a state of genuine molecular resolution.

The caution: what LTB4 told us about non-healers

The non-healer story required a different approach. We assessed lipid mediators (small molecular signals involved in initiating and resolving inflammation) comparing healer and non-healer wounds in the combined treatment group. Most showed no significant difference between the two groups. One, however, stood out: leukotriene B4, or LTB4. Non-healers had significantly lower LTB4 levels than untreated controls.

 

Under normal conditions, LTB4 is the signal that recruits neutrophils - the immune system’s first responders - to swarm a site of infection, form dense clusters, and neutralise pathogens. It is a critical component of antimicrobial defence. In diabetes, this immune machinery is already compromised. Our hypothesis is that the anti-inflammatory cytokines in the cord blood serum may have further dampened this response in some animals during the early post-injury window, while the amniotic membrane scaffold may have provided a hospitable surface for biofilm formation. In animals with already-diminished immune capacity, the result was a biological environment tipped towards infection rather than healing.

 

This does not negate the promise of the combined treatment. But it does flag something important for clinical translation: patient selection and infection monitoring will be critical. The same biological properties that make cord blood serum a powerful anti-inflammatory regenerative agent could, in a subset of patients with highly compromised immune function, work against them.

What this means going forward

Taken together, the data suggests that the combined application of cord blood serum and amniotic membrane leads to meaningfully better healing quality than either product alone; not just in terms of wound closure speed, but in the depth of tissue regeneration that determines long-term outcomes. The proteomic data provides molecular confirmation of what the histology showed visually: these wounds weren’t just closed; they were resolved.

 

Further research is needed to understand the mechanisms driving failure in the non-healers, and to determine whether this infection risk translates to humans in the same way. The interplay between diabetes-related immune dysfunction, the anti-inflammatory effects of the treatment, and biofilm susceptibility is complex - and important to untangle before this approach reaches the clinic at scale.

 

For me, contributing the proteomic analysis to this work was one of the more personally meaningful applications of the technology. Proteomics gives you a window into biology that no other technique quite matches: not just what happened, but the molecular story of why.

 

And now, every time I think back to those cord blood banking brochures, I think about the chain of connection: a donation made at a moment of new life, processed and preserved, contributing (potentially) to research that could spare someone else the devastating experience of a wound that refuses to heal.

 

My son has finally gone quiet. The sway is working. And somewhere in the dark, I find that rather satisfying.

 

How Trace Labs can help

Studies like this one illustrate something important: the questions that matter most in biomedical research often can't be answered by a single technique. Understanding whether a wound has truly healed - not just at the surface, but at a molecular level - requires the kind of deep proteomic insight that tells you what thousands of proteins are doing, and what that means biologically.

 

That's exactly where Trace Labs comes in. I provide high-throughput, high-resolution proteomics analysis and interpretation for researchers across academia and industry. Whether you're investigating wound healing, metabolic disease, cancer biology, or any field where the molecular detail matters, I have the expertise and the analytical rigour to turn complex biological samples into meaningful data.

 

If you're working on research that could benefit from proteomics, or if you're simply not sure whether it could, I'd love to have a conversation with you. Contact me at mare@tracelabs.co.za.

 

The article “Combined therapeutic use of umbilical cord blood serum and amniotic

membrane in diabetic wounds” was published in Biochimie (Elsevier), Volume 227, 2024, pages 193–204.

 

Authors: C. Montague, Y. Holt, M. Vlok, P. Dhanraj, K. Boodhoo, M. Maartens, K. Buthelezi, C.U. Niesler, M. van de Vyver.

 

Conducted at Stellenbosch University and sponsored by Next Biosciences (Pty) Ltd.

 

Full paper: doi.org/10.1016/j.biochi.2024.07.012